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Behavioral and psychological symptoms of dementia (BPSD), constitute a major clinical component of Alzheimer’s disease (AD). There is a growing interest in BPSD as they are responsible for a large share of the suffering of patients and caregivers, and they strongly determine the patient’s lifestyle and management. Better detection and understanding of these symptoms is essential to provide appropriate management. This article is a consensus produced by the behavioral group of the European Alzheimer’s Disease Consortium (EADC). The aim of this article is to present clinical description and biological correlates of the major behavioral and psychological symptomatology in AD. BPSD is not a unitary concept. Instead, it should be divided into several symptoms or more likely: groups of symptoms, each possibly reflecting a different prevalence, course over time, biological correlate and psychosocial determinants. There is some clinical evidence for clusters within groups of BPSD. Biological studies indicate that patients with AD and BPSD are associated with variations in the pathological features (atrophy, brain perfusion/metabolism, histopathology) when compared to people with AD without BPSD. An individually tailored approach taking all these aspects into account is warranted as it may offer more, and better, pharmacological and non-pharmacological treatment opportunities.
Genetic epidemiology explores the interrelationship of genetic and environmental risk factors in which genes are measured indirectly in ways that reflect aggregate effects "averaged" across the entire genome. This chapter describes the principles and methodology of psychiatric genetics using four-paradigm framework: basic genetic epidemiology, advanced genetic epidemiology, gene finding, and molecular genetics. Each of these paradigms has strengths and limitations, and they are in a process of dynamic interaction with each other. Genetic epidemiology has proved a reliable method to answer basic questions about the overall importance of genetic risk factors for psychiatric illness. The advanced genetic epidemiology paradigm has been used to study the relationships between neuroticism and depression. Molecular genetics is an entirely laboratory-based discipline applying a range of modern methods from genomics to neuroscience to try to identify and then trace pathophysiological pathways.
Alzheimer's disease (AD) is an example of cortical dementia, where most of the pathological changes lie in cortical association areas and the predominant clinical features are symptomatic of cortical dysfunction. The differential diagnosis of AD is complex and is usually made in two stages: diagnosis of the dementia syndrome and diagnosis of the underlying etiology. Each of these stages is complicated by the existence of conditions that mimic dementia in presentation and by the risk of inappropriately diagnosing AD where other conditions are responsible for the dementia state. Despite the fact that the concept of dementia, in terms of a decline in cognitive function and behavioral change, has existed for many years, there is still a general lack of agreement about the components of the syndrome. This article reviews the issues surrounding the differential diagnosis of the dementia syndrome and explores the points of differentiation between AD and some similar etiologies encountered when making a differential diagnosis.
Patients with dementia with lewy bodies (DLB) have progressive deficits in cognition, parkinsonism, and neuropsychiatric symptoms. Cholinesterase inhibitors have been used to ameliorate cognitive decline and neuropsychiatric symptoms in short-term trials. In this study, patients with DLB were treated with rivastigmine up to 96 weeks. Improvement from baseline was seen in cognitive function as measured by the Mini-Mental State Examination (MMSE), and neuropsychiatric symptoms as measured by the Neuropsychiatric Inventory (NPI) over the first 24 weeks of treatment. By 96 weeks, neither the MMSE scores nor the NPI scores were significantly worse than at baseline.
Dementia with Lewy bodies (DLB) is a common cause of the dementia syndrome. Symptomatic treatment of the fluctuating cognition, visual hallucinations, and sleep distrubance that characterize this condition is challenging; neuroleptics are relatively contraindicated. We describe eight patients fulfilling the consensus diagnostic criteria for probable DLB who were treated with rivastigmine. Clinical features rated were: cognition by the Modified Mini-Mental State Examination (3MS); and behavioral and psychiatric symptoms by the Neuropsychiatric Inventory (NPI). Additional information was obtained from family and nursing reports. Seven patients showed resolution or improvement in cognition and neuropsychiatric symptoms as demonstrated by improvement in their 3MS and NPI scores. They also became more independent in mobility and activities of daily living, and the majority returned to live in their own home. Of the seven patients with sleep disruption, six improved. One case had no improvement in his symptomatology and the rivastigmine was stopped. Outcomes in this case series suggest that rivastigmine is well tolerated in clinical practice.
Dementia with cortical Lewy bodies (LBD) was first described by Okazaki et al in 1961 and is now recognised as a relatively common cause of the dementia syndrome. The true prevalence of LBD is unknown. In post-mortem studies of patients diagnosed as having dementia in life, the mean frequency of Lewy body dementia is 12.5% (Byrne, 1997). Clinically diagnosed LBD (using operational clinical criteria) is found in 10–23% of patients presenting to, or in the care of, psychogeriatric services (Collerton et al, 1996). What is not yet certain is its nosological status; opinion is divided between regarding it as a variety of Alzheimer's disease (the Lewy body variant), a distinct disease (senile dementia of the Lewy body type) or a spectrum disorder related to both Parkinson's disease and to Alzheimer's disease (Byrne, 1992).
It is difficult to estimate the frequency with which etiologies other than AD and cerebrovascular disease (vascular dementia) cause the dementia syndrome. There are problems in the uncritical acceptance of frequency estimates based on autopsy series (Byrne, Smith & Arie, 1991) as such samples are usually highly selected, and pathological diagnosis, until recently, has been less than reliable. Other factors such as the medical specialty from which the autopsy sample was derived have been shown to influence the frequency with which different etiologic causes for the dementia syndrome occur (Jellinger et al., 1990). AD is more common in autopsy samples referred by psychiatrists, whereas Parkinson's disease is most frequently found in samples referred by geriatricians and physicians. Galasko et al. (1994), found that 12% of their sample of (predominantly) community residents with dementia who came to autopsy had non-AD, nonvascular dementia.
Epidemiological studies of dementia rarely consider differential diagnosis and those that do are largely limited to AD and vascular dementia (Hofman et al., 1990). We do know the prevalence of some of the individual conditions that cause dementia and in some instances have information on how frequently this occurs. For example, the prevalence of Parkinson's disease is 2% of the population aged over 70 years (Schoenburg, 1987) and dementia arises in around 15–20% of these patients (Brown & Marsden, 1984; Mayeux et al., 1988). Lishman (1987) lists 39 non-AD, nonvascular causes of dementia and McKeith (1994) lists 42 other dementias.
In a four-year follow-up study of 1042 elderly people (aged 65 years or older), randomly sampled from the community, levels of dementia were assessed using a two-phase case-finding procedure (screening followed by clinical interview) among survivors. Clinical information on those not reinterviewed was provided by death certificates, hospital case notes, or postal questionnaires. The weighted four-year cumulative incidence of dementia was 3.7% (95% confidence intervals: 2.4%-5.0%), with age-specific rates of 0.9%, 2.8%, 5.2%, 9.0%, and 8.7% for the age groups 65–69, 70–74, 75–79, 80–84, and 85–89 years respectively. While consistent with data from other British regions, it remains likely that these rates underestimate true incidence.