Is dementia a mental illness?

OBJECTIVE: To examine whether dementia is a mental illness. METHOD: An analysis of decisions in the Supreme Court of New South Wales that dementia per se was not a mental illness in terms of the 1958 Mental Health Act. A brief review of the extrusion of other diseases from psychiatry. RESULTS: Concepts in legislation are based on a dichotomy between mental infirmity and mental illness that has changed over time. This change is the result of shifting perceptions about the basis of illness and disease and the causation of mental symptoms. Mental health legislation is aimed as much at social control of feared behaviour as protecting the ill/incompetent. Guardianship legislation offers a more holistic response that better meets the patient's needs and could be extended to supplant mental health legislation. CONCLUSIONS: Dementia's departure from mental illness reflects psychiatry's continuing marginalization within medicine on an outdated mind/body or illness/disease split. This underlines one of the psychiatrist's roles as the vehicle to 'medically' explain abnormal behaviour. This model means that behaviour, once explained in terms of disease as opposed to illness, can be moved from the direct responsibility of psychiatry into other areas of medicine. Paradoxically, this suggests that the future of psychiatry will be in a completely different direction from its current biological focus.     

Towards a prevention of dementia?

Many studies have shown that high blood pressure and, to a lesser extent, other vascular risk factors could be the target of interventions aiming to reduce the incidence of dementia. Two large controlled trials have demonstrated that blood pressure lowering drugs have a significant effect on the risk of dementia including Alzheimer's disease. On another hand, large epidemiological studies have shown associations between different vascular factors and dementia. Overall, these data suggest that interventions aiming to reduce the level of vascular risk factors might prevent dementia. The expected benefit of these interventions could be estimated from data provided by epidemiological studies, but large population-based controlled studies are needed to demonstrate the efficacy of preventive interventions.     

Is late onset depression a prodrome to dementia?

BACKGROUND: Recent research suggests there are clinical and biological differences between late onset depression (LOD) and early-onset depression (EOD). OBJECTIVES: In this paper we review clinical, epidemiological, structural neuroimaging and genetic investigations of late life depression that have been performed over the past two decades and offer evidence that LOD is often a prodromal disorder for dementia. RESULTS: LOD patients are more likely to have cognitive impairment and to have more deep white matter lesions (DWMLs). Evidence concerning cortical and temporal lobe atrophy is conflicting, while the ApoE 4 allele is not associated with LOD. CONCLUSIONS: It is likely that LOD is not a prodrome for a particular type of dementia, but the majority of patients who do develop dementia will acquire Alzheimer's disease (AD) or a vascular dementia, as these are by far the most common causes of dementia. This issue requires further clarification with follow-up of patients over the long term.     

Alcohol-related dementia: a 21st-century silent epidemic?

Evidence suggests a J-shaped relationship between alcohol consumption and cognitive impairment and other health indicators, with low levels of consumption having better outcomes than abstention or moderate to heavy drinking. Most research to date has focused on the protective effects of drinking small amounts of alcohol. As alcohol consumption is escalating rapidly in many countries, the current cohort of young and middle-aged people may face an upsurge of alcohol-related dementia. The dangers of heavy drinking and its effect on cognition require further attention.     

Disruptive vocalizations: a means to communicate in dementia?

Disruptive vocalizations (DVs) constitute a serious problem in geriatric nursing homes. The current literature suggests that DV can be interpreted as a way for demented persons with language limitations to communicate with others. In an attempt to test this hypothesis, 59 participants were recruited from six nursing homes to form two groups: one group of individuals with preserved language skills (PLS) and another group with altered language skills (ALS). They were compared on the frequency and types of DV. The results indicate that individuals with ALS manifest DV at a greater frequency than those with PLS. These persons also present a greater number of distinct DV forms. The results are interpreted in terms of language deterioration associated with dementia.     

Are subjective cognitive complaints a risk factor for dementia?

The objective is to evaluate the prognosis of subjective cognitive complaints (SCC) patients during 4-year follow-up. A prospective study on 92 SCC patients investigating their cognitive, affective and behavioural aspects. SCC patients were classified as having no objective cognitive impairment (NOCI), mild cognitive impairment (MCI), or subtypes of MCI. Results: 43 patients were found to have NOCI and 49 MCI. During the follow-up, 45.5% of NOCI patients remained unchanged, 13.9% were diagnosed as MCI and only one progressed to dementia. Of the MCI patients, 32.3% remained stable, 18.4% became demented and 4% reverted to NOCI. Visual attention, behavioural memory, long-term verbal memory, apathy and caregiver distress, provided independent predictors of progression to dementia.     

Parkinson's disease dementia: what's in a Lewy body?

This brief review deals with pathological aspects of dementia associated with Parkinson's disease (PDD). PDD has been variably linked with cortical Lewy body topography and density. alpha-Synuclein and Alzheimer-type pathology frequently co-exist, suggesting that a combination of pathology related to protein dysmetabolism, possibly with synergistic protein-protein interaction, underpins the cognitive impairment in PDD. Dementia may therefore ensue when a "toxic threshold" is reached, irrespective of the combination of pathologies involved in reaching that threshold. The nature of this putative protein-protein interaction needs to be further elucidated, and also whether there are specific clinical correlates of the pathological substrate. Serum and cerebrospinal fluid proteins or imaging techniques may be useful in future as biomarkers to identify the relative contribution of Lewy-related and Alzheimer-type pathology in a given case of PDD and to inform the rational use of drugs that can reduce alpha-synuclein aggregation and beta-amyloid production.     

Cost-effectiveness of a collaborative dementia care management—Results of a cluster-randomized controlled trial

IntroductionThe purpose of this study was to determine the cost-effectiveness of collaborative dementia care management (DCM).MethodsThe cost-effectiveness analysis was based on the data of 444 patients of a cluster-randomized, controlled trial, conceptualized to evaluate a collaborative DCM that aimed to optimize treatment and care in dementia. Health-care resource use, costs, quality-adjusted life years (QALYs), and incremental cost per QALY gained were measured over a 24-month time horizon.ResultsDCM increased QALYs (+0.05) and decreased costs (?569€) due to a lower hospitalization and a delayed institutionalization (7 months) compared with usual care. The probability of DCM being cost-effective was 88% at willingness-to-pay thresholds of 40,000€ per QALY gained and higher in patients living alone compared to those not living alone (96% vs. 26%).DiscussionDCM is likely to be a cost-effective strategy in treating dementia and thus beneficial for public health-care payers and patients, especially for those living alone.     

Does a wander garden influence inappropriate behaviors in dementia residents?

BACKGROUND: The effect on resident behaviors of adding a wander garden to an existing dementia facility was investigated. METHODS: 34 male residents were observed for 12 months before and after opening the garden. Behaviors were assessed using the Cohen-Mansfield Agitation Inventory Short Form (CMAI), incident reports, as needed medications (pro re nata [PRN]), and surveys of staff and residents' family members as indices of affect. RESULTS: Final CMAI scores and total PRNs employed were lower than baseline values with a trend for residents who used the garden more often to have less agitated behavior. Verbal inappropriate behaviors did not change significantly whereas physical incidents increased. Staff and family members felt that the wander garden decreased inappropriate behaviors and improved mood and quality of life of the dementia residents. CONCLUSIONS: Study design characteristics and garden management may have affected behaviors both positively and negatively. Additional studies are needed to explore the benefits of wander gardens for dementia residents.     

HIV—dementia

Brain-derived neurotrophic factor (BDNF) is a promising candidate for the gene therapy of neurological disease. To deliver BDNF to neurons of the central nervous system (CNS), a nucleotide sequence encoding the mature peptide of BDNF was inserted into the genome of poliovirus, a neurotropic virus that is known to replicate mainly in motor neurons of the spinal cord of the CNS. Thus, the recombinant poliovirus constructed was replication-competent. The expression of BDNF in cultured cells infected with the recombinant poliovirus was evident when the cells were analyzed using an immunofluorescence assay and Western blotting. When the recombinant viruses were injected intramuscularly into transgenic mice that carry the human poliovirus receptor gene, the antigens of poliovirus and BDNF were detected in the motor neurons of the spinal cord at 3 days postinfection, and had disappeared by 7 days postinfection. This study suggests that poliovirus can be used as a virus vector for the delivery of neurotrophic factors to the motor neurons of the central nervous system and may provide a new approach for the treatment of motor neuron diseases.     

What do we know about dementia?: a survey on knowledge about dementia in the general public of Japan

OBJECTIVE: The importance of early detection of dementia has been highlighted in recent years by the medical and scientific community; however, delays often occur between the recognition of signs or symptoms and a decision by the patient or family to seek professional help. Such delays may be caused by a lack of knowledge about dementia among patients and family members. The aim of this study was to determine the understanding of dementia among the general public. METHODS: We conducted a survey in Japan that asked 11 questions regarding knowledge of 'general' information, 'symptoms', and 'biomedical' issues related to dementia. A quota sampling method was used to select 2,500 participants, 2,115 of who were eligible for the analyses. RESULTS: The average number of correct responses among females was significantly greater than that among the males. A multiple comparisons test demonstrated that middle-aged women were more knowledgeable than younger and older respondents. It was revealed that there was a lack of knowledge on biomedical aspects of dementia, i.e. cause, treatment, and prognosis along with a misunderstanding of dementia as senescence forgetfulness among the general public. CONCLUSIONS: There appeared to be gaps in knowledge on dementia among the general public, which may prevent caregivers from planning upcoming social and financial challenges. Correct information needs to be given by health professionals and care staff. Educational initiatives planned for the general public could be useful, and should target those groups, men and non-middle aged women who have lower knowledge.     

Is subcortical vascular dementia a clinical entity for clinical drug trials?

Several therapeutic trials have been performed for vascular dementia, with drugs differing in type and mechanism of action. The results have been almost invariably inconclusive. Given the current notion that there are different subtypes of vascular dementia according to pathophysiological mechanisms, it is reasonable to suspect that one of the main causes of the disappointing results was that the study samples included patients not fitting with the rationale of selective treatments. Testing this hypothesis is difficult because characterization of patients in relation to different subtypes of vascular dementia is not available for most studies. However, attempts are ongoing to reclassify patients entered in some trials for post hoc subgroup analyses with some preliminary interesting results. We propose that (1) specific subtypes of vascular dementia should be the target in any single trial using a treatment with a proper rationale; and (2) subcortical vascular dementia, caused by small vessel disease leading to lacunar infarcts and subcortical white matter changes, represents a clinically and radiologically well-defined entity to be considered for future trials designed specifically for testing adequate drugs.     

Semantic dementia and primary progressive aphasia: a problem of categorization?

The relationship between semantic dementia (SD) and primary progressive aphasia (PPA) has been the subject of debate ever since the syndromes were first described, in converging streams of research from the neuropsychological and neurologic communities. The most salient clinical features of SD are anomia with circumlocution and semantic paraphasia, single-word comprehension deficit, and reduced category fluency. Of critical importance is the fact that patients also show deficits on non-verbal tasks using visual, auditory, and other modalities, suggesting that the key impairment in SD is a breakdown in conceptual knowledge rather than a specific problem with language. The finding of item consistency between the various tests supports this view. The order in which the features appear can be explained by the variable degree of redundancy in access to semantic knowledge from the different perceptual modalities. Atrophy is seen in the anterior and inferior temporal lobe rather than in classic language areas, further distancing SD from aphasic syndromes. Semantic dementia and progressive non-fluent aphasia (PNFA) share some clinical and pathologic characteristics with frontal variant frontotemporal dementia, but there are also clear differences between the three syndromes. We believe that many patients described as having fluent primary progressive aphasia in fact have early SD. Semantic dementia is a well-defined syndrome, distinct from PNFA but related to it within the spectrum of frontotemporal lobar degeneration syndromes.     

Is the immobility of advanced dementia a form of lorazepam-responsive catatonia?

Patients with end-stage dementia typically are very immobilized. Could this state actually be a form of lorazepam-responsive catatonia? Catatonia has been documented following cerebrovascular accidents, head injury, HIV encephalitis, brain tumors, and multiple sclerosis. Identified anatomical substrates include frontal lobes, parietal lobes, limbic system, diencephalon, and basal ganglia. Given that Alzheimer's disease, vascular dementia, Lewy body dementia, corticobasal degeneration, frontotemporal dementia, and Parkinsonian dementia often have degeneration in some of the same areas, dramatic awakenings might be possible by giving lorazepam challenges to locked-in dementia patients. If even a small percentage were lorazepam responders, the impact worldwide would be tremendous. Serious consideration should be given to undertaking large-scale clinical trials.     

Inflammation and depression: Is there a causal connection with dementia?

Epidemiological studies show that there is a correlation between chronic depression and the likelihood of dementia in later life. There is evidence that inflammatory changes in the brain are pathological features of both depression and dementia. This suggests that an increase in inflammation-induced apoptosis, together with a reduction in the synthesis of neurotrophic factors caused by a rise in brain glucocorticoids, may play a role in the pathology of these disorders. A reduction in the neuroprotective components of the kynurenine pathway, such as kynurenic acid, and an increase in the neurodegenerative components, 3- hydroxykynurenine and quinolinic acid, contribute to the pathological changes. Such changes are postulated to cause neuronal damage and thereby predispose chronically depressed patients to dementia.