5 Steps to Reverse Dementia

Unraveling Alzheimers Disease

Unraveling Alzheimers Disease

I leave absolutely nothing out! Everything that I learned about Alzheimer’s I share with you. This is the most comprehensive report on Alzheimer’s you will ever read. No stone is left unturned in this comprehensive report.

Get My Free Ebook


The Great Brain Secret

This DVD shows the secret to getting back all of your brain strength and giving you the mental power and memory of a much younger person. You can learn the 60 second trick that will regrow your brain cells and get rid of all of your senior moments and give you the mental power that you have always needed. Family members have said of people that have done this program that it is like getting their grandparent back. If you find that you have trouble remembering your grandchildren's names or important dates or anniversaries, this course is for you. You will remember everything that you forgot, and have the memories that you used to not be able to form. If you already have signs of forgetfulness, you are on a dangerous path that could eventually lead to you forgetting almost everything. If you act soon, you can get your mind to all the strength that it is supposed to have!

The Great Brain Secret Summary

Rating:

4.6 stars out of 11 votes

Contents: DVD Video
Creator: Walter Bailey
Price: $37.00

My The Great Brain Secret Review

Highly Recommended

Furthermore, if anyone else has purchased this product or similar products, please let me know about your experience with it.

I feel totally comfortable and confident in recommending The Great Brain Secret knowing it can be so helpful if you fully apply what they share.

Download Now

Principle 2 Comorbidity Is Common in Dementia

In discussing interdisciplinary teams and how models of functioning can lead to conflicts, Lichtenberg (1994) reported that whereas the medical model emphasizes a ruling out ' ' of influences until a diagnostic entity is determined, the psychosocial model emphasizes a ruling in of influences on behaviors. In applying the psychosocial model to dementia, psychological practitioners need to be aware of the relatively common occurrence of comorbidities. Depression often accompanies dementia. Delirium occurs more frequently among those with dementia. Environmental stresses, such as caregiver burden, relocation, boredom, or overstimulation, can heighten behavioral disturbances among those with dementia. Caregiver functioning impacts the care recipient's cognitive and noncognitive behaviors. Further, as the disease progresses, so do comorbidities. Thus, memory decline is associated with functional decline, risk of delirium episodes, and loss of independence in self-care abilities. These...

Alzheimers Disease And Atherosclerosis

There is some evidence that chronic activation of T cells, leading to increased proliferation and telomere shortening, may be involved in other age-related diseases as well. The etiology of Alzheimer's disease (AD) is not known, but our recent studies suggest a possible involvement of T cells. We observed that the telomere length of T cells, but not of B cells or monocytes, correlates with mental function tests in AD patients (Panossian et al., 2002). Those patients with lower Mini Mental Status Examination (MMSE) scores, which is a marker of disease status, had T cells with shorter telomeres than those persons with higher MMSE scores. These findings suggest that the immune system of AD patients is perturbed in some way and may not necessarily respond normally to therapeutic vaccines aimed at retarding AD disease progression. Interestingly, one such therapeutic vaccine trial was recently interrupted due to unanticipated brain inflammation in some participants (Nicoll et al., 2003).

Management Of Dementiapsychiatric Principles

As is evident throughout this volume, the management of patients with dementia is a challenge that spans time as well as an interdisciplinary approach. Psychiatric management requires simultaneous attention to psychiatric syndromes, both clear-cut and mixed comorbid medical illnesses social supports family dynamics and both pharmacologic and nonpharmacologic interventions. The following principles are useful anchors to the effective diagnosis and management of those psychiatric syndromes that complicate dementia illnesses.

Psychological Functioning In People With Intellectual Disabilities Mental Illness And Dementia

'Dementia', on the other hand, usually occurs after a period of normal functioning and involves 'the global impairment of higher cortical functions' (Royal College of Physicians, 1981), affecting memory, thought, language, emotion, personality and behaviour, as well as motor and sensory abilities. Dementia may arise from a number of underlying conditions, but the most frequent causes in 'elderly' people (i.e. persons aged 65 years or more), such as Alzheimer's disease (the commonest form), are progressive and irreversible (see Jacoby and Oppenheimer, 2002 Gelder et al., 2000, for further details).

Psychological Evaluation and Nonpharmacologic Treatment and Management of Alzheimers Disease

Alzheimer's disease (AD), the most common form of dementia, is estimated to affect 4 million people in the United States and up to 15 million people worldwide. This neurodegenerative disorder is characterized by progressive loss of memory and other cognitive functions, which impairs social and occupational functioning. AD is the number one cause of disability in the elderly because it is not directly fatal and survival is long (about 10 years from diagnosis). Over the past decade, most medications approved for the treatment of AD work via cholinergic stimulation and target the symptoms of attention and memory. These treatments are not thought to affect the progression of disease, and current research for new drugs focuses on agents that target the characteristic neuropathological features of neuritic plaques composed of amyloid and neurofibrillary tangles composed of tau protein. While significant effort from the public sector and industry is focused on the biological aspects of the...

Diagnostic Assessment Of Alzheimers Disease

There are currently no guidelines to suggest routine screening of the elderly for dementia, and the clinical evaluation usually begins with a complaint either from the patient or from an observer. Because changes in cognition and memory, which are the most common early signs of AD, can be caused by many medical conditions, especially in the elderly, it is critical that such complaints be evaluated by a medical professional. For the diagnosis of AD, two broad areas must be evaluated cognition and functioning. History, one of the most important tools of evaluation, should focus on characterizing the nature of the cognitive change, the rapidity with which it occurs, and the presence of important medical or life events occurring in proximity to the cognitive change. The other area to assess is functional ability, particularly function impaired by cognitive loss. Areas to address include difficulty handling financial matters, instrumental tasks such as shopping, chores, food preparation,...

Natural Models Of Alzheimerlike Pathology

Information on the neurobiology of aging in nonhuman primates has grown steadily over the past four decades (Hof et al., 2002). By far the most thoroughly investigated species are the rhesus monkey (Macaca mulatta) and the squirrel monkey (Saimiri spp), although there is a burgeoning literature on other nonhuman primate species, including great apes, marmosets (Saguinus jacchus), cynomolgus monkeys (Macaca fascicularis), green monkeys (Chlorocebus aethiops), baboons (Papio hamadryas), and mouse lemurs (Microcebus murinus). We will focus here primarily on rhesus monkeys and squirrel monkeys as natural primate models of Alzheimer-like pathology. Rhesus monkeys. Rhesus monkeys are Old World monkeys with a maximum life span of approximately 40 years they reach puberty at 3-4 years of age, and females go through menopause at approximately 25 years of age (Walker, 1995). Age-related cognitive decline is well-documented in rhesus monkeys, but a dementia-like state has not been reported....

Nonpharmacological Approaches To Treating Alzheimers Disease

Behavioral cognitive disturbances may result from a number of factors including cognitive change and neurobiological and environmental factors. Behavioral symptoms associated with dementia and AD are vast and include wandering, aggression, agitation, illusions, delusions, hallucinations, sleep disturbances, suspiciousness, paranoia, tearfulness, verbal outbursts, and mood disturbances. Common cognitive symptoms associated with AD include memory loss, confusion, spatial disorientation, thinking deficits, and reasoning difficulties. To determine the best technique, it is important to consider stage of disease and specific behavioral symptoms. Certain behaviors may be more amenable to change than others without the use of medication.

Progress In Recapitulating Alzheimers Disease

The original models for AD attempted to mimic the neurochemical deficits, mainly in the cholinergic pathways. With a better understanding of the neuropatholog-ical lesions at a molecular level, transgenic models were devised that recapitulated a surprising degree of AD pathology. These include reasonably faithful age dependence, brain region specificity, and appropriate behavioral effects. There is evidence of neuroinflammation in microglial activation, even though many of the mouse strains are deficient in the inflammatory response (Schwab et al., 2004). There is also evidence of oxidative stress, and some of the neurochemical changes are similar to those in AD. Some of the behavioral changes in the APP overexpressing mice also resemble facets of early AD dementia.

Neurologic Aspects of Dementia with Lewy Bodies and Parkinsons Disease with Dementia

The two most common neurodegenerative disorders in the elderly are Alzheimer's disease (AD) and Parkinson's disease (PD). While each has well-defined clinical and pathologic features and specific criteria for clinical and pathological diagnosis, some degree of overlap between these two disorders exists. Some AD patients develop extrapyramidal signs and symptoms characteristic of PD, some patients with typical PD develop a dementia, and both disorders can co-occur in the same individual. This, however, does not explain all or even most of the cases of PD with dementia. Another entity known as dementia with Lewy bodies (DLB) has been estimated to account for 15 to 20 of late-onset dementias and has been only more recently recognized as the second most common cause of dementia after AD (McKeith, Perry, & Perry, 1999 McKeith et al., 1996). In this chapter, we focus on the dementias associated with both DLB and PD with dementia.

Dementia With Lewy Bodies Historical Perspective

In 1961, Okazaki, Lipkin, and Aronson, published the first case reports of two individuals who presented at ages 69 and 70 with dementia and severe extrapyramidal rigidity who, on autopsy, demonstrated diffuse Lewy body (LB) pathology in the cerebral cortex. Between the early 1960s and 1984, 34 similar cases were reported in Japan by Dr. Kosaka, who coined the term DLB in 1978. The term was used to describe the typical distribution of LB in the cortex and subcortical regions (Kosaka, Yoshimura, Ikeda, & Budka, 1984). In subsequent reports over the next decade, many more cases were recognized at autopsy. DLB is not a new disorder, but it has only recently been recognized due largely to the improvement in tissue staining techniques, which allowed for enhanced visualization of the LB in the cortex. On reexamination of postmortem material collected in Newcastle-upon-Tyne during the 1960s, it was revealed that 17 had cortical LB. More recent reports have found that approximately 10 to...

Dementia Pseudodementia

Course over 24 hours Insight Orientation Memory loss Responses to mistakes Dementia (chronic organic brain syndrome) The incidence of dementia increases with age, affecting about 1 person in 10 over 65 years and 1 in 5 over 80 years. The important causes of dementia are degenerative cerebral diseases including Alzheimer's disease (60 ) The DSM-III (R) criteria for dementia are presented in Table 8.2 and clinical clues suggesting dementia in Table The many guises of dementia can be considered in terms of four major symptom groups. 6

Management of dementia

There is no cure for dementia the best that can be offered to the patient is tender loving care. Education, support and advice should be given to both patient and family. Multidisciplinar evaluation and assistance are needed. Regular home visits by caring sympathetic people are important. Such people include relatives, friends, general practitioners, district nurses, home help, members of a dementia self-help group, religious ministers and meals on wheels. The sufferers tend to manage much better in the familiar surroundings of their own home and this assists in preventing behaviour disturbance.

Neuropsychological Dysfunction in Parkinsons Disease Without Dementia

In reviewing the PD literature, Lieberman (29) reported that 17 to 53 of treated and untreated PD patients without dementia demonstrate cognitive dysfunction. Unfortunately, few of the studies reported formal criteria for determining what did or did not constitute dementia, thus making it difficult to determine whether patients were in the early stages of dementia. As noted earlier, more recent studies suggest that formal neuropsychological testing may uncover mild cognitive deficits in 25 to 36 of PD patients at the time of diagnosis (22,23). When present in early PD, cognitive dysfunction is typically mild and most commonly involves bradyphre-nia (a slowness of thought) and subtle deficits in executive functions, recall, and or visuoperceptual spatial functions (30).

Neuropsychological Dysfunction in Parkinsons Disease with Dementia

The annual incidence of clinically diagnosed dementia in PD (PDD) is about 3 for individuals younger than 60 years and 15 or less for those 80 years and older (66,67). Estimates of dementia prevalence in patients with PD vary between 9 and 93 , depending on which diagnostic criteria, ascertainment methods, and sampling methods are implemented (24). The methodologically soundest studies yield prevalence estimates of about 25 (68). Dementia is very rarely present early in the disease course moreover, dementia that precedes or accompanies the evolution of motor symptoms should raise concern that the dementia might be related to factors other than PD, for example, AD, LBD, or depression. Recently revised diagnostic criteria for LBD (69) propose that the clinical diagnostic term PD with dementia be reserved for individuals who have a clinical diagnosis of PD and have had only motor symptoms for at least 12 months before developing fluctuating cognition and other neuropsychiatric symptoms...

Prevalence Of Dementia In Idiopathic Pd

Deficits are ubiquitous in PD however, the incidence of frank dementia tends to be much lower. Prevalence rates of dementia reported in the literature range from 4 to 93 . Cummings (1988) calculated a mean prevalence of 39.9 based on 4,336 cases reported in the literature, whereas Brown and Marsden (1984) have suggested that 15 to 25 might be a more valid estimate. Prevalence figures must be viewed with caution and vary widely depending on what subpopulation is included (early versus late onset), what diagnostic criteria are used for dementia, and to what degree potential confounds of motor dysfunction are taken into account. Most studies examine heterogeneous PD samples, collapsing across disease duration, age, and motor symptom severity and treatment regimens. One factor that appears to be consistently important in determining which parkinsonian patients become demented is age.

Clinical Features of PD with Dementia

Celesia and Wanamaker's 1972 study was one of the first to show that older patients exhibit a higher incidence of cognitive impairment and overall dementia compared with younger parkinsonians, and they also exhibit a more rapid course of disease progression. This was subsequently supported by other investigators using standardized neuropsychological tests. Mayeux et al. (1988) found a 40 frequency of dementia in PD patients older than 65 years. Dubois, Pillon, Sternic, Lhermitte, and Agid (1990) studied a group of early-onset (< 45 years) and late-onset PD compared to age-matched controls. Early-onset PD exhibited mild memory problems and cognitive slowing, but late-onset exhibited more global cognitive dysfunction. But some have criticized these studies for examining only one point in time, thus bypassing the question of whether the older subjects were nondemented in their younger years and deteriorated with advancing age. Biggins et al. in 1992 conducted serial assessments on 87...

Neuropsychological Characteristics of Dementia in PD

Cognitive disturbances may range from relative circumscribed deficits to global dementia. Mild cognitive deficits are common in idiopathic Parkinson's disease (IPD) and are characterized by impaired cognitive flexibility, psychomotor slowing, reduced ability to learn and retrieve new information, and impaired visuospatial skills. The concept of subdividing dementias on clinical grounds into cortical and subcortical dementias has been adapted by many in the field as a clinically useful concept, but others remain critical of this notion. The concept of subcortical dementia was originally based on an analysis of the pattern of personality and cognitive deficits in PSP (Albert, Fledman, & Willis, 1974) and Huntington's disease (HD Folstein et al., 1975 see Table 3.2). The majority of studies addressing the concept of subcortical dementia have used PD as the prototypic subcortical dementia and AD as the prototypic cortical dementia. The term subcortical dementia originally applied to...

Risk Factors for Dementia in Parkinsons Disease

TABLE 3 Risk Factors for Dementia in Parkinson's Disease Lower socioeconomic status Family history of Parkinson's dementia patients with PD on verbal fluency, attentional, and visuospatial tasks was associated with subsequent development of dementia. Woods and Tr ster (93) found that nondemented PD patients who met criteria for dementia at one-year follow-up evaluation demonstrated poorer baseline performance on measures of word-list learning and recognition, complex auditory attention, and executive function.

Neurologic Aspects of Prion Diseases and Frontotemporal Dementias

The degenerative dementias discussed in this chapter are the human prion diseases and the frontotemporal dementias (FTDs). These dementias are often termed atypical dementias because of their unique clinical and pathological features when compared to more common causes of dementia such as Alzheimer's disease and vascular dementia. Both prion diseases and FTD are rare, but as a group, these atypical degenerative dementias are frequently encountered in clinical practice. Practitioners need to be knowledgeable of the unique issues that arise in the diagnosis and management of patients' suffering from these dementias. There have been significant advances in our understanding of pathophysiology of these diseases in the past 10 years, and there is hope that effective disease-modifying treatments can be developed in the future. This chapter reviews these developments and our current understanding of how to diagnose and treat patients suffering from these unusual dementias.

Frontotemporal Dementia

Our understanding of the epidemiology of frontotemporal dementia (FTD) has been limited by confusion and controversy in what constitutes FTD both clinically and pathologically. The original descriptions of the prototypic FTD, Pick's disease, occurred in a series of papers between 1892 and 1906 by Arnold Pick. Pick described several patients with prominent behavioral disturbances and expressive language impairments that had very circumscribed atrophy of the frontal lobes. Alois Alzheimer described the histopathology in 1911, identifying swollen achromatic cells (Pick cells) and argyrophilic inclusions (Pick bodies). However, by the 1970s neuropathologists had established that some cases resembling Pick's disease clinically did not have Pick cells and Pick bodies at autopsy (Constantinidis, Richard, & Tissot, 1974). It is now clear that many patients with clinical symptoms resembling Pick's disease lack classic Pick's disease pathology. Multiple names have been used to describe such...

And HIVAssociated Dementia

Neuronal injury and apoptosis may account, at least in part, for neurological complications associated with human immunodeficiency virus (HIV)-1 infection ranging from mild cognitive and motor impairment to dementia. The primary cell types infected in the brain are macrophages and microglia. These cells have been found in vivo and in vitro to release neurotoxic factors. Evidence has accumulated that neuronal apoptosis in HIV-related insults occurs predominantly via an indirect pathway comprising a complex cooperation of cytokines, reactive oxygen species and reactive nitrogen species, lipid mediators, and excitotoxins. These molecules lead to excessive stimulation of the N-methyl-d-aspartate subtype of glutamate receptor (NMDAR). Of note, chemokine receptors, which, in conjunction with CD4, mediate HIV infection of macrophages microglia, are present on neurons and astrocytes in addition to macrophages microglia. Thus, these receptors potentially allow direct interaction between the...

Psychological and Neuropsychological Aspects of Lewy Body and Frontal Dementia

Recognition of non-Alzheimer's dementias has become essential for experts in geriatrics. Unfortunately, many laypersons and even general practitioners equate the terms Alzheimer's and dementia. In fact, as many as two-thirds of Alzheimer's disease (AD) patients have a coexisting condition (Lim et al., 1999), making pure AD far less common than was once thought. This chapter reviews the more common other dementia, including mixed dementia, which is the co-occurrence of AD and vascular dementia Lewy body dementia, which most often occurs in conjunction with AD pathology and frontotemporal dementia, a group of non-Alzheimer pathologies with focal atrophy of the frontotemporal areas. Within each of these dementias, we review the literature on the epidemiology, diagnostic standards, clinical diagnostic practices, symptoms, and interventions of these dementias. Accurate differential diagnosis of dementia is critical for discerning its pathophysiol-ogy, understanding the relationship between...

Pathophysiology of Dementia

There is controversy regarding which features are the primary contributors to dementia in PD. PD is characterized by cell loss in the substantia nigra pars compacta (SNc), resulting in loss of dopaminergic input into the striatum. Several pathological and functional imaging studies have shown that in PD, there is greater depletion in the lateral compartment of the SNc, which projects to the putamen, than in the medial compartment, which projects to the caudate (139-141). Cognitive impairment is associated with loss of dopaminergic projections to the caudate (142). This functional division of the striatum is, perhaps, the main reason for the predominance of motor, over cognitive symptoms in PD and is likely why dopaminergic agents do not markedly improve cognition in PD (143). A relationship between cholinergic deficiency and dementia in PD has also been reported (144). Striking cell loss is seen in the nucleus basalis of Meynert, which provides projections to the amygdala and...

Gsk3 Regulation And Alzheimers Disease

Since its discovery, GSK-3 has been found to be involved in many physiological process. GSK-3 plays important roles in embryonic development, cell differentiation, microtubule dynamics, cell cycle division, cell adhesion, glucose metabolism, and apoptosis 19,20 . In addition, a growing amount of experimental data has demonstrated its involvement in some pathological processes as Alzheimer's disease.

Summary of Frontotemporal Dementia

The database and knowledge of FTD that has accumulated in only 20 years of research is impressive. Unlike MD and LBD, FTD does not occur concurrently with AD pathology. Rather, it is defined as a group of non-Alzheimer's dementias with focal atrophy of the frontotemporal areas. Subsyndromes include frontal lobe dementia (FLD), Pick's disease, motor neuron disease with dementia, progressive nonfluent aphasia, and semantic aphasia. Important characteristics of FTD make these dementias more dissimilar from AD than are MD and LBD. First, the pathological changes of FTD more focally affect the frontal and anterior temporal regions, whereas the pathological changes of AD typically begin in the hippocampus and posterior temporal and parietal regions and eventually may nonselectively impair much of the subcortical and cortical areas of the brain. FTD may also affect the brain asymmetrically, unlike more global dementias such as AD, VaD, MD, and LBD. Second, a genetic etiology of FTD is more...

Parkinsons Disease Dementia

Pathological findings considered to account for dementia in PD include severe pathology in monoaminergic and cholinergic nuclei that project to the cortex producing a subcortical dementia (39 ), coexistent Alzheimer's disease (AD) (29 ), and diffuse cortical Lewy bodies (26 ) (22). The basal forebrain cholinergic system is the subcortical region most often implicated in dementia, and neurons in this region are damaged in both AD and Lewy body dementia. Neuronal loss in the basal nucleus is consistently found in PD, especially PD with dementia (23). Cholinergic deficits are common in PD (24) and they may contribute to dementia in PD in those cases that do not have concurrent AD or cortical Lewy bodies. While virtually all PD brains have a few cortical Lewy bodies (22), they are usually neither widespread nor numerous in PD patients who were not demented. Several studies have shown, however, that cortical Lewy bodies are numerous and widespread in PD with dementia (25-27) and that the...

Guam Parkinsondementia Complex

A characteristic parkinsonism with dementia Parkinson dementia complex (PDC) with a number of features that overlap with PSP (50) has been reported in the native Chamorro population of Guam since the 1950s (51). The frequency of PDC is declining in recent years for unknown reasons, and the etiology is unknown. The gross findings in PDC are notable for cortical atrophy affecting frontal and temporal lobes, as well as atrophy of the hippocampus and the tegmentum of the rostral brainstem (52). These areas typically have neuronal loss and gliosis with many NFTs in residual neurons.

Lacunar Dementia Inferior Genu Dementia

The clinical picture is characterized by sudden change in cognition, associated with fluctuating attention, memory loss, confusion, abulia, psychomotor retardation, inattention, and other features of frontal lobe dysfunction but with mild focal findings such as hemiparesis or dysarthria (Pantoni et al., 2001 Tatemichi, Desmond, Prohovnik, et al., 1992 Tatemichi, Desmond, & Prohovnik, 1995). Lacunar dementia is usually due to a single lacunar stroke involving the inferior genu of the internal capsule, causing ipsilateral blood flow reduction to the inferomedial frontal cortex by a mechanism of diaschi-sis (Chukwudelunzu, Meschia, Graff-Radford, & Lucas, 2001 Mori, 1998). This lesion in the genu of the inferior capsule may sever corticothalamic and

Senile dementia of Alzheimer type SDAT Epidemiology

SDAT accounts for over half of all cases of dementia in old age. It is present in 5 per cent of people over age 65 and 20 per cent of people over 80. Women are affected nearly twice as often as men, probably mainly reflecting women's longer lifespan. AD is also the commonest of the primary 'presenile' dementias, with onset earlier in life, say, between the ages of 40 and 60. changes neuronal loss, senile plaques, and neurofibrillary tangles. Neurons are decreased both in number and size, and astrocytes proliferate. Senile plaques, which have argyrophilic cores containing an amyloid-like substance, develop in the grey matter. Nerve fibres form tangles called Alzheimer's neurofibrillary degeneration. Lewy bodies (see below) may also be present. Onset is gradual over a year or more. Loss of recent memory is usually the first symptom, and is followed by deterioration in other mental functions, emotional lability or sustained depression, and personality change. Delusions and...

Psychological and Neuropsychological Aspects of Vascular and Mixed Dementia

Vascular dementia (VaD) has been estimated to range from the second to the fourth most common form of dementia. Similar to Alzheimer's disease (AD), VaD is a clinical diagnosis that is confirmed only on autopsy. Unlike the clinical criteria for AD, however, there is wide variability in the clinical criteria established to diagnose VaD. Coupling that with autopsy studies showing that most clinical cases of VaD turn out to be mixed dementias or even AD (Nolan, Lino, Seligman, & Blass, 1998), it is clear that VaD is an area full of controversy. This chapter reviews the clinical criteria for VaD, explores the relationship between stroke and dementia and the relationship between cognitive deficits and vascular disease, and then delves into the area of mixed dementia.

Transmissible spongiform encephalopathies prion dementias

These are rare forms of dementia, caused by accumulation of abnormal prion proteins in the brain. Prion stands for proteinaceous infectious particle, a unique form of infective agent, as it contains no genetic material. Prions are now accepted as the cause of a group of transmissible spongiform encephalopathies including scrapie (in sheep), chronic wasting disease (in deer), and bovine spongiform encephalopathy (BSE) ('mad cow disease'). In some families, these dementias appear to be due to an inherited prion gene mutation, which follows an autosomal dominant pattern. Other cases are infective, due to an abnormal prion protein acquired in various ways. The disorders can be transmitted to experimental animals, and human cases have followed neurosurgery, corneal grafting, or administration of cadaveric growth hormone. Dementia, accompanied by myoclonus or ataxia, usually starts in middle life. EEG changes are characteristic, and diagnosis can be confirmed by finding a prion gene...

Diagnostic Criteria For Vascular Dementia

Four major clinical criteria are used in the diagnosis of VaD. The National Institute of Neurological Disorders and Stroke Association Internationale de Recherche et l'Ensignement en Neurosciences (NINDS-AIREN) criteria contain explicit statements about the diagnosis of dementia, the evidence for stroke, and the relationship between stroke and dementia (Rom n et al., 1993). Dementia, using this criteria, is defined as memory impairment and impairment in two other cognitive domains (i.e., language, attention, visuospatial skills, executive functioning). Cerebrovascular disease is defined by focal signs on neurological exam and evidence of stroke by brain imaging. Finally, there must be a relationship between the dementia and the vascular disease. The second clinical criteria in use are the California Alzheimer's Disease Diagnostic and Treatment Center (ADDTC) criteria for ischemic VaD (Chui et al., 1992). Dementia is defined as a deterioration from a prior level of functioning, and...

Cognitive Differentiation Of Vascular And Alzheimers Dementia

The most common studies of cognition in VaD have been attempts to distinguish it from AD. This line of research has most often investigated whether semantic abilities in AD are worse than in those with VaD and whether the deficits noted in VaD cases are consistent with a frontal-subcortical dementia (Mast, MacNeill, & Lichtenberg, 2002). A number of studies have attempted to differentiate dementia groups via cognitive patterns and overall abilities. These are reviewed more thoroughly in the Mast et al. study. Overall, the studies suffer from several methodological deficiencies. First, most of the studies use small sample sizes and, therefore, are underpowered. Second, and perhaps most importantly, the MMSE is used as a control for overall levels of dementia. The use of a screening measure to control for overall level of impairment is problematic. It is no surprise, then, that the results of the studies reviewed by Mast and colleagues exhibit no clear pattern. Mast et al. (2002)...

Neurologic Aspects of Nondegenerative Nonvascular Dementias

Although dementia is most often the result of a degenerative or vascular disease, there are almost innumerable other causes of dementia. These other dementias, albeit less common, are important because many may be improved or stabilized with early recognition and treatment. This chapter highlights some of the infectious, toxic metabolic, hydrocephalic, neoplas-tic, traumatic, and demyelinating etiologies of dementia. Epidemiological studies provide varying estimates for the relative frequency of specific dementias. Frequency estimates may be influenced dramatically by the characteristics of the population studied (age, geographic location, community vs. referral basis) and the diagnostic methods employed (clinical vs. pathologic). Sultzer and Cummings (1994) compiled data from 34 studies of dementia in 3,587 patients. As shown in Table 8.1, the conditions discussed in this chapter, when combined, may explain fewer than 15 of all cases of dementia. In certain populations, however, one...

Psychiatric Diagnosis and Management of Psychosis in Dementia

Alzheimer's disease (AD), the predominant form of dementia, comprises 60 to 80 of all cases of dementia (Stoppe et al., 1999). The number of patients with AD represents a growing public health problem that may reach crisis proportions in the future. In 1993, the estimated AD population in the United States was approximately 4 million, and it is estimated to reach 14 million by the year 2050 (Tariot, Podgorski, Blazina, & Leibovici, 1993). AD has been defined as the neurodegenerative illness with the most neuropsychiatric sequelae, including behavioral dyscontrol and psychosis. Behavioral complications and psychosis during AD constitute a tremendous burden to caregivers and are common precipitants of institutionalization (Burns, Jacoby, & Levy, 1990 Cohen et al., 1993 Deimling & Bass, 1986 Weiner, Alexander, & Shortell, 1996). Antipsychotic medications are the treatment of choice for psychosis or behavioral complications associated with dementia (Helms, 1985 Schneider,...

Psychiatric Assessment and Treatment of Depression in Dementia

The interface of depression and dementia is a challenging but critical area in the assessment and treatment of dementia. The traditional focus of this interface has been an emphasis on avoiding the misdiagnosis of dementia in elderly patients having depression with associated cognitive impairment, so-calledpseudodementia. However, it is increasingly recognized that a more common and often more difficult clinical quandary is accurately diagnosing depression in existing dementia (Draper, 1999). Depressive symptoms and syndromes are frequent in already-established cases of dementia, complicating clinical management, exacerbating functional difficulties, and creating other negative outcomes. Recent studies have also investigated whether depression may be a prodromal symptom of or an independent risk factor for the development of dementia. This chapter focuses on depression occurring in the three most common types of dementia Alzheimer's dementia (AD), vascular dementia (VaD), and diffuse...

The Issue Of Pseudodementia

Historically, much emphasis has been given to the distinction of depression from dementia in late life. The term pseudodementia has long been used to denote the cognitive impairment that occurs with depression which reverses with adequate treatment of mood symptoms. However, more recent studies have revealed that many cases of so-called pseudodementia either have cognitive deficits that do not remit despite clinical recovery (Abas, Sahakian, & Levy, 1990) or are found to have irreversible cognitive impairment on follow-up. In one study, up to 50 of geriatric patients with reversible dementia were found to have irreversible dementia at five-year follow-up (Alexopoulos, Meyers, Young, Mattis, & Kakuma, 1993). In another study, depressed mood in elderly community-dwelling residents without dementia was associated with a significantly increased risk of dementia diagnosis at follow-up of one to five years (Devanand et al., 1996). Butters et al. (2000) found that elderly nondemented...

Gsk3 In Alzheimers Disease

GSK-3 has been associated with several neuropathological mechanisms involved in Alzheimer's disease. The postmortem diagnosis of Alzheimer's rests on the presence of two abnormal deposits extracellular plaques consisting of P-amyloid (AP), and intracellular neurofibrillary tangles (NFTs). Compared to age-matched control samples, increased levels of GSK-3 have been found in postmortem analysis of brains from Alzheimer's disease patients 8 . In addition GSK-3 has been shown to localize to pretangle neurons, dystrophic neurites, and NFTs in Alzheimer's disease brain 8 . Neurons actively undergoing granulovascular degeneration are also immunopositive for active GSK-3P 9 . A spatial and temporal pattern of increased active GSK-3P expression coinciding with the progression of NFT and neurodegeneration have been demonstrated. Taken together, these studies provide strong evidence that the active form of GSK-3 P is increased in Alzheimer's disease brain. Recently it has been demonstrated,...

Dementia Delirium and Cognitive Status

Overall, reported rates for dementia among older adults have ranged from 4 to 7 (Pfeffer, Afifi, & Chance, 1987), although more recent studies have estimated rates as high as 10 (Evans et al., 1989). The rates increase with age, with estimates of 3-5 among adults aged 65 to 74,18-20 of those aged 7584, and as many as 50 of those aged 85 and older. It has been estimated that as much as 90 of dementia is of the Alzheimer's type, with another 10 accounted for by vascular dementia (Evans et al., 1989 Tatemichi, Sacktor, & Mayeau, 1994). In comparison to non-Hispanic whites, however, the rates of vascular dementia among African Americans, Chinese Americans, and Japanese Americans, appear to be 2-4 times higher, as a result of higher rates of conditions such as hypertension, whereas the rates among Hispanics are lower, a result of lower rates of cardiovascular disease (Hasegawa, Homma, & Imai, 1985).

Dementia delirium and other organic brain syndromes

A woman of 83 had been diagnosed as suffering from moderate to severe dementia of Alzheimer's type, but was able to remain at home because of the devoted care of her 62-year-old daughter. Her behaviour became much more agitated and confused over a period of 2 days, alternating with periods of drowsiness her urine had become foul-smelling over this time. The GP and community psychiatric nurse diagnosed acute-on-chronic confusion due to urinary tract infection, and continued to look after the patient at home, for her daughter wished to avoid hospital admission. With antibiotics, a change of catheter, and some sedation with small doses of chlorpromazine, the patient's condition returned to normal over a few days. Her daughter nevertheless appeared exhausted, and regular respite care admissions were arranged to ease her burden.

Psychological and Nonpharmacological Aspects of Depression in Dementia

The relationship between depression and dementia has been one of intense scientific and clinical interest over the past twenty years. Raskind (1998) summarized the major ideas about how depression relates to dementia 1. Depression is either a prodrome or a risk factor for dementia. 2. Depression complicates dementia through the direct contribution to excess disabilities. By far, the most intense scientific attention is given these days to the debate as to whether depression is a prodrome of dementia, specifically Alzheimer's disease (AD), or whether depression is instead a risk factor for the development of AD or other forms of dementia. This chapter is divided into five sections. In the first section, we explore the evidence for and against the question of depression as risk factor or prodrome. In addition to providing the empirical evidence and interpreting whether it supports either or both concepts, we present information on the vascular depression hypothesis and how this...

Depression And Excess Disability In Dementia The Activity Limitation Framework

A major issue of scientific and clinical importance to understanding dementia is determining in what ways depression affects cognitive and noncognitive symptoms. Family caregivers report that the noncognitive symptoms of dementia (e.g., apathy, agitation) have greater impact on the family unit's day-to-day life than do the cognitive symptoms of dementia (Riley & Snowden, 1999). Of concern, then, is how depressive syndromes affect the behaviors of the person with dementia and whether depression should be an area of intense intervention, not only to remove the depressive symptoms but to forestall excess disabilities in persons with dementia. One conceptual framework to use in assessing these issues is the activity limitation framework. The activity limitation framework was developed from research data that focused on medically ill elders (Williamson, 1992 Williamson & Schulz, 1995). Physical illness, pain, functional abilities, and depression were investigated cross-sectionally...

Depression in Dementia Effects on Cognition

Our understanding of whether the presence of depression in persons with dementia, particularly in those with AD, is associated with excess cognitive disabilities is limited. Ross, Arnsberger, and Fox (1998) reported that although a group of depressive and nondepressive patients with AD had similar MMSE scores, cognition was significantly related to depression diagnosis beyond psychosocial and demographic predictors. Their study, from the California Alzheimer's Disease Cooperative, consisted of 183 patients with depression and 1,300 nondepressed patients. The authors concluded that depression contributes to cognitive excess disabilities. These findings have been reported by others as well (see Lichtenberg, Ross, Mills, & Manning, 1995, for a review). Of greater interest more recently has been whether there is a specific pattern of cognitive excess disability in depressed persons with dementia. Wefel, Hoyt, and Massman (2000) compared 37 depressed Alzheimer's patients with 98...

Phenomenology Of Depression In Dementia

Understanding the unique aspects of depression in dementia can assist clinicians and researchers in the detection and treatment of this syndrome. Lazarus, Newton, Cohler, Lesser, and Schweon (1987) were one of the earlier research groups to examine the phenomenology of depression in dementia. In their investigation of 44 persons with dementia, 18 participants were diagnosed as depressed via the Hamilton Rating Scale. Interrater reliability was .68 for this study. The authors reported that those items associated with inner states of despair were far more common than were vegetative symptoms. Thus, mood, anxiety, and hopelessness were noted to be particular aspects of depression in those with dementia. Much of the data following the Lazarus group's study has supported their initial findings. Katz (1998) and Verhey and Visser (2000) have specified that mood disorders appear to be more prominent in those with preclinical and those with mild dementia. Verhey and Visser examined a group of...

Assessment Of Depression In Dementia

Depression is a syndrome, a constellation of symptoms that potentially has many etiologies. In this chapter, we are focused on depression in persons with dementia and have discussed two conceptual frameworks that help explain depression onset the vascular depression and activity limitation frameworks. The Diagnostic and Statistical Manual of Mental Disorders, fourth edition (DSM-IV APA, 1994), codes depression in persons with dementia as 290.13 dementia with depressed mood, including those with major depressive disorder. Implicit in this diagnosis is the consideration of minor depressive disorder. Minor depression is listed in the DSM-IV appendix but is not currently a DSM-IV-coded diagnosis. Minor depression, however, is subsumed under 290.13, the code for dementia with depressed mood as defined previously. The major distinctions between major and minor depression are typically not found concerning mood but the number of vegetative symptoms that are experienced (sleep, appetite,...

Nonpharmacological Treatment For Depression In Dementia

Nonpharmacological treatment for depression in dementia has focused on the dyad of both the caregiver and the person with dementia. In a randomized controlled trial of short-term supportive counseling aimed at reducing caregiver burden (not depression in persons with dementia), Mittelman, Ferris, Shulman, Steinberg, and Levin (1996) reported that the intervention led to delayed nursing home admissions for the person with dementia. The most rigorous research on improving depression in persons with dementia through nonpharmacological treatments comes from Teri and colleagues at the University of Washington. This work is based heavily on Lewinsohn's behavioral theory of depression. Lewinsohn and Graf (1973) reported on cross-sectional data of younger, middle age, and older adults who kept a record of mood ratings and daily events. The authors noted that mood fluctuated widely and was significantly related to the number of pleasurable events that individuals engaged in. In summary, the...

Other genes for Alzheimers disease

There have been multiple strategies deployed to try to map these additional AD-susceptibility genes. Genetic linkage studies and family-based association analyses have been employed on datasets with pedigrees multiply affected with AD, and have led to the suggestion that there may be additional susceptibility loci in (1) the pericentro-meric region of chromosome 12 (Alzheimer Type 5) (Pericak-Vance et al., 1997 Rogaeva et al., 1998) and (2) the long arm and pericentromeric region of chromosome 10q (Alzheimer Type 6) (Bertram et al., 2000 Ertekin-Taner et al., 2000 Myers et al., 2000). However, to date, the exact genes in these regions that cause susceptibility to AD have not been identified. Weaker evidence, in single studies have also implicated chromosome 20p (Olson et al., 2002) 15q22 (Scott et al., 2003) and 9p (Pericak-Vance et al., 2000). The glutathione S-transferase omega-1 (GSTO1) gene on distal chromosome 10q has also been implicated as a gene modulating age-of-onset in both...

Familial nonspecific dementia

A small number of pedigrees have been described which segregate an autosomal dominant adult-onset disease characterized by early-onset dementia with non-specific neuropathological changes of neuronal loss, minor gliosis and some spongiform change (Gydesen et al., 1987). Completely absent are the typical findings of Alzheimer's disease (AD) or Pick's disease. Genetic linkage studies have mapped one such disease locus in one large Danish pedigree to a 12 cM region of chromosome 3 spanning the centromere between the markers D3S1284 and D3S1603 (Brown etal., 1995).

Frontotemporal lobe dementia FTD

Fronto-temporal dementia is a pleomorphic neuro-degenerative illness which typically begins before the age of 65 years. In a minority of cases, the disease is inherited as an autosomal-dominant trait (Lynch et al., 1994 Wszolek et al., 1992). The disease often begins with personality and behavioral changes including disinhibition manifest by alcoholism, hyper-religiosity, hypersexuality, hyperphagia (elements of the Kluver-Bucy syndrome) and stealing. As the disease progressed in these families, further abnormalities in judgment, language and praxia developed. In addition to these cognitive changes, some patients also developed Parkinsonism and amyotrophy. However, presentations with primary progressive aphasia, Parkinsonism, dystonia and or oculomotor disturbances are not infrequent. Neuropathologically, the illness is typified by fronto-temporal atrophy with severe neuronal loss, spongiform change in the superficial layers Genetic linkage studies in the subset of FTD cases showing...

Familial British dementia FBD and familial encephalopathy with neuronal dementia with neuroserpin deposits

Recently, two very rare forms of inherited dementia (Familial British dementia and familial encepha-lopathy with neuroserpin inclusion bodies (FEN1B)) have been described which support the emerging concept that many of the inherited dementias are disorders of protein processing in which there is either intracellular or extracellular toxic accumulation of misfolded misprocessed proteins, a theme common to all of the diseases discussed here. Familial British dementia is characterized by spasticity, ataxia, and later progressive dementia accompanied by widespread demyelination, with distinctive perivascular fibrous deposits that are clearly different from the plaques of AD. A T > A transversion mutation in the stop codon of the BRI Missense mutations in neuroserpin, a neuron-specific serine protease inhibitor (serpin), have been described in two pedigrees with a familial dementia (Davis etal., 1999). In these families with FEN1B the mutant neuroserpin forms typical serpin loop-sheet...

Diffuse Lewy Body Dementia DLBD

The diagnosis of depression in dementia is complicated by several factors overlap symptoms, the question of symptom persistence, cohort effect, ageist myths, communication difficulties in later stages of dementia, ag-nosonosia, and reliability of caregiver reports (Thorpe & Groulx, 2001).

Age Related Hippocampa Dysfunction Early Alzheimers Disease vs Normal Aging

As we age, all of us will experience an inexorable slide into forgetfulness. Age-related memory decline localizes, in part, to the hippocampal formation, a brain circuit made up of separate but interconnected hippocampal subregions. Human studies have established that Alzheimer's disease targets the hippocampal circuit early in its course, and since Alzheimer's disease affects older individuals it is one cause of age-related hippocampal dysfunction. Animal studies, however, have established that the aging process itself targets the hippocampal circuit, contributing to age-related hippo-campal dysfunction observed in all mammalian species. These independent observations have led to a continued debate among investigators of the aging human brain, summarized by the following questions Is age-related hippocampal dysfunction in humans etiologically homogeneous, or is age-related hippocampal dysfunction caused by both AD and by normal aging If age-related hippocampal dysfunction is caused...

Psychiatric Assessment and Treatment of Nonpsychotic Behavioral Disturbances in Dementia

In addition to core cognitive and functional deficits, neuropsychiatry symptoms, emotional disorders, and behavioral alterations are ubiquitous among patients with dementia syndromes. Clinicians should be concerned with the behavioral signs and symptoms of Alzheimer's disease (AD) and other dementias because they are prevalent, distressing to the patient, and upsetting to caregivers. Often they contribute significantly to the need for institutional care. A previous cross-sectional multicenter study of several hundred outpatients with AD found that no patient had been free of behavioral signs or symptoms in the preceding month (Tariot, Mack, et al., 1995). A population-based study of dementia found a point prevalence of psychopathology of more than 60 and asserted that the lifetime risk of psychopathology for a patient with dementia approached 100 (Lyketsos et al., 2000). These figures make clear that it is important to know how to recognize and manage the behavioral manifestations of...

Neurobiological Mechanisms of Psychosis in Dementia

Based on neuroimaging studies, an association between delusions in dementia and dysfunction in the paralimbic area of the frontal cortex has been found (Sultzer, 1996). Using neuropathological and neuochemical investigations in patients with primary dementia, those with psychosis have been found to have significantly more plaques and tangles in the medial temporal-prosubicular area and the middle frontal cortex (Zubenko et al., 1991) and four to five times higher levels of abnormal paired helical filament (PHF)-tau protein in the entorhinal and temporal cortices (Mukaetova-Ladinska, Harrington, Roth, & Wischik, 1993). A decrease in serotonin in the prosubiculum of the cerebral cortex was found in psychotic versus nonpsychotic dementia patients (Lawlor, Ryan, & Bier-rer, 1995 Zubenko et al., 1991). Acetylcholine decreases in function have been correlated with increased thought disorders (Sunderland et al., 1997), and cholinergic agents have been observed to decrease the emergence...

Summary of Lewy Body Dementia

Although pathologically distinct from Alzheimer's disease, LBD usually occurs in combination with the neurofibrillary tangles and plagues of AD, suggesting an etiological connection between these two forms of dementia with variations in alertness and attention, recurrent well-formed and detailed visual hallucinations, or spontaneous motor symptoms of parkinson-ism. Other criteria symptoms suggestive of LBD are repeated falls, syncope, transient loss of consciousness, neuroleptic sensitivity, systematized delusions, and hallucinations in modalities other than visual. Postmortem studies indicate these criteria are highly specific but not particularly sensitive to identifying true cases of LBD. Missed cases are most often diagnosed either pure AD or VaD. The lack of distinction between LBD and AD is certainly complicated by their frequent co-occurrence and their similarly affected brain regions. On the other hand, misdiagnosed cases of LBD as MD may, in part, reflect clinicians' being...

Assessment of Psychosis in Alzheimers Disease

Et al., 1994), NPI NH (Wood et al., 2000), Behavioral Pathology in Alzheimer's Disease (BEHAVE-AD Reisberg, 1984), the Gottfries-Brane-Steen Scale (Gottfries, Brane, & Steen, 1982), CERAD Behavior Rating Scale (Tariot et al., 1995), the Cohen-Mansfield Agitation Inventory (Cohen-Mansfield et al., 1989), and the Columbia University Scale for Psychopathology (CUSPAD) (Devanand et al., 1992). The NPI is a caregiver-based instrument (Cummings et al., 1994) that has become widely used in the research setting. The NPI is a valid and reliable means of assessing neuropsychiatric symptoms (e.g., agitation, apathy, depression, anxiety, delusions, hallucinations, irritability, and delusions) in patients with dementia, with a decision tree approach making it very useful (Cummings & McPherson, 2001). The NPI's psychometric properties include strong reliability and validity established in a number of studies and a variety of settings and demonstrated sensitivity to change in several clinical...

Alzheimers disease

Alzheimer's disease, or AD, is a progressive, incurable disease of the brain caused by the degeneration and eventual death of neurons (nerve cells) in several areas of the brain. Patients with AD first lose such mental functions as short-term memory and the ability to learn new things. In the later stages of AD they gradually lose control over their sense of orientation, their emotions, and other aspects of behavior. End-stage AD is characterized by loss of control of body functions, an increased likelihood of seizures, loss of the ability to eat or swallow, and eventual death from infection or malnutrition. Alzheimer's disease is the most common cause of dementia (loss of cognitive abilities) in the elderly it is thought to be responsible for 50 -70 of cases of dementia in the United States. Alzheimer's disease was first identified in 1906 by a German psychiatrist and neuroanatomist named Alois Alzheimer. He was studying slides prepared from the brain of a fifty-one-year-old woman,...

Lewy Body Dementia

In 1961, Okazaki and colleagues first described diffuse Lewy bodies in two demented patients with parkinsonism and psychiatric symptoms. Lewy body dementia may rarely occur as a pure disease or, more commonly, in combination with AD or Parkinson's disease. Numerous terms have been used, including diffuse Lewy body dementia, Lewy body variant of AD, and Parkinson's disease with dementia (Drachman & Swearer, 1998). The generic term, dementia with Lewy bodies (LBD), is recommended by the Consortium on Dementia with Lewy bodies (McKeith et al., 1996) and is used in this chapter. The pure form of diffuse Lewy body dementia is rare (Holmes, Cairns, Lantos, & Mann, 1999 Mega et al., 1996) because the majority of cases with LBD have significant number of plaques that are morphologically indistinguishable from those found in AD cases. Mild to severe AD pathology was found in 81 of clinical LBD cases (Londos, Passant, Brun, & Gustafson, 2000). It is not understood whether these cases...

Dementia

Cognitive impairment is common in PD, especially in the domain of executive function (28). Such deficits are usually the earliest cognitive signs in PD (117). Patients or caregivers often report difficulties with decision making, planning, and completion of goal-directed behaviors. When these cognitive deficits worsen, and patients have impairment of occupational or social functioning, a diagnosis of dementia is made (13). At this point, it is unclear whether the presence of early cognitive deficits leads to dementia. The rate of cognitive decline in PD can be variable depending upon the population subset. A recent community-based study estimated that the mean overall annual rate of cognitive decline in PD patients was one point on the Mini-Mental State Examination (MMSE) (118). However, patients with PD and dementia declined faster, at a rate of 2.3 points, whereas PD patients who did not develop dementia progressed at the same rate as age-matched controls. Complicating the picture...

Poststroke Dementia

In addition to the previous forms of strategic single-stroke dementia, the most common form of poststroke VaD is MID, occurring when dementia develops after multiple strokes. The incidence of poststroke dementia is ascertained by performing cognitive tests after stroke (typically, at three months postictus). According to Tatemichi et al. (1990), Pohjasvaara et al. (1997), and Barba et al. (2000), the most important risk factors for poststroke VaD are older age, lower educational level, recurrent stroke, left hemisphere stroke (associated with a fivefold increase in risk of developing poststroke dementia, an effect not explained by aphasia), as well as presence of dysphagia, gait limitations, and urinary impairment. Patients with poststroke VaD are more often current smokers and have lower blood pressure and orthostatic hypotension. Larger periventricular white matter ischemic lesions by MRI are also predictive of poststroke dementia. Moroney and colleagues (1996) observed that hypoxic...

Thalamic Dementia

A mechanism similar to the one mentioned previously probably underlies the so-called thalamic dementia of vascular origin (Castaigne et al., 1966) caused by large bilateral paramedian thalamic polar infarcts (Bogous-slavsky, 1995) and some cases of caudate stroke (Caplan et al., 1990). Lesions involve the anterior (polar) thalamus in territories irrigated by the polar thalamic artery, a branch of the posterior communicating artery or, the medial and central thalamus involving the dorsomedial nucleus and the mamillothalamic tract (Van der Werf, Witter, Uylings, & Jolles, 2000). These last two structures are irrigated by the paramedian thalamic artery, a branch of the basilar-PCA. The critical lesion in the production of thalamic amnesia is the damage of the mamillothalamic tract that projects into the anterior nuclei of the thalamus, and then to the cingulate cortex (Bogous-slavsky, Regli, & Uske, 1988 Van der Werf et al., 2000). All patients present with depressed level of...

Vascular dementia

Vascular dementia (VaD) is common it frequently co-exists with AD. Epidemiology Lewy body dementia Definition and neuropathology Comparatively recently, in fact since the last edition of this book, Lewy body dementia (LBD) has been recognized as a distinct condition. This is a type of dementia in which Parkinsonian features are prominent. Conscious level and cognitive function tend to fluctuate and visual illusions or hallucinations may occur, as may frank psychotic symptoms. It has been recognized that Parkinson's disease can sometimes proceed to dementia. Patients with LBD seem to be on a continuum between pure Parkin-sonism, on the one hand, and dementia on the other hand. It is not yet clear what proportion of dementia cases overall should be classified as LBD. Clearly, this would depend on how a case should be defined. It has, however, been suggested that it is the second commonest cause of dementia after AD.

Stroke And Dementia

Several studies have linked stroke to dementia onset. Tatemichi et al. (1992) studied 251 hospital patients with ischemic stroke, as well as a group of medical controls. Twenty-six percent of the stroke patients became demented within three months as compared to only 5 of the medical controls. Correlates of dementia onset included age, lower levels of education, and African American race. Censori et al. (1996) studied 304 consecutive stroke admissions, of which 146 individuals met the criteria for first stroke. Twenty-five percent of the sample became demented within three months. The strongest predictors of dementia onset in this sample were presence of diabetes, atrial fibrillation, aphasia, and middle cerebral artery infarcts. Findings from the nun study, however, give pause as to whether infarcts cause the dementia or whether the infarct uncovered or accentuated an already-existing neuropathological condition (Snowdon et al., 1997). Snow-don hypothesized that members of the...

HIV dementia

Cognitive impairment is associated with HIV infection and AIDS. However, it is difficult to generalize about the prevalence of dementia, as the outlook for the condition varies greatly between countries where there is good health care and those where access to AIDS drugs is limited and the outlook much poorer. Regarding the UK, the predictions at the start of the epidemic of very large numbers of HIV-dementia cases have fortunately proved wide of the mark.

Mixed Dementia

Recognition of non-Alzheimer's dementias has become essential for experts in geriatrics. Unfortunately, many laypersons and even general practitioners equate the terms Alzheimer's and dementia. In fact, as many as two-thirds of Alzheimer's patients have a coexisting condition (Lim et al., 1999), making pure Alzheimer's far less common than was once thought. This section reviews the more common other dementias, including mixed dementia, which is the co-occurrence of Alzheimer's and VaD. Within mixed dementia, we review the literature on the epidemiology, diagnostic standards, clinical diagnostic practices, symptoms, and interventions of these dementias. Accurate differential diagnosis of dementia is critical for discerning their pathophysi-ology, understanding the relationship between coexisting dementia, and developing disease-specific treatments for distinct forms of dementia.

Dementia Pugilistica

An akinetic-rigid syndrome with dysarthria and dementia is sometimes a long-term outcome of repeated closed-head trauma, as seen in professional boxers. The pathology on gross examination, other than lesions that can be attributed to trauma, for example, subdural membranes and cortical contusions, is nonspecific. The substantia nigra may also show pigment loss. Microscopically, there are NFTs similar to those in AD in the brainstem monoaminergic nuclei, cortex and hippocampus and some cases also have amyloid plaques (55,56). At the electron microscopic level, they are composed of paired helical filaments and biochemically composed of 68, 64, and 60 kDa forms (57).

Alzheimers Dementia

There is wide variation in prevalence estimates for major depression in AD, ranging from 0 to 86 (Burns, Jacoby, & Levy, 1990 Wragg & Jeste, 1989). This variation likely reflects several factors population studied ( lower in community and neurological settings than psychiatric inpatient or nursing home settings), diagnostic approaches (Diagnostic and Statistical Manual of Mental Disorders DSM criteria, rating scales, caregiver report, etc.), dementia stage, exclusion of patients with prior depression, as well as symptom overlap between depression and dementia (Lazarus et al., 1987 Meyers, 1998). Some (Pearlson et al., 1990 Rovner et al., 1989) but not all (Migliorelli et al., 1995) investigators have found an association of depression in dementia with a positive family history of depression. Lyketsos et al.'s (Lyketsos et al., 1996) study reported this association, but only in women, and found no relationship between risk for depression in AD and younger age at AD onset or...

Causes of dementia

Common causes of dementia include Alzheimer's disease (common, dominant memory impairment with gradual decline). Vascular dementia (fluctuating course ). Dementia with parkinsonism (e.g. Lewy body dementia). Creutzfeld-Jakob disease (rare, rapid decline, myoclonus though this can be seen in other dementias ). Treatable causes of dementia include

Principle 1 Accurate Assessment of Both Cognitive Abilities and Noncognitive Behaviors Is Based on Thorough Knowledge

The assessment of cognition and, in particular, memory loss, has been found to be one of the most sensitive measures of early cognitive decline and dementia. Psychological techniques include the valid interpretation of thorough psychometric testing. Whereas it is common in physician offices to use very brief mental status measures (e.g., Mini-Mental State Exam) to document cognitive decline, psychological techniques more thoroughly assess cognitive functioning and, in particular, domains of cognitive functioning. As a result, neuropsychological assessment measures are typically more sensitive, specific, and provide better positive and negative predictive power than do screening exams alone (Becker, Boller, Lopez, Saxton, & McGonigle, 1994). While these instruments can be quite powerful, there are many caveats to their proper usage and interpretation. All cognitive assessment is based on a deficit model in which one individual's score is typically compared to a range of normative...

Principle 3 Treatment Interventions Should Be Based on Conceptual Frameworks and Tested Empirically to Determine

Behavioral and psychosocial interventions with persons with dementia and with family and professional caregivers are based on the conviction that persons with dementia, similar to those with any chronic disease, can have an improved quality of life. Because dementia attacks both cognitive and noncognitive aspects of functioning, interventions are geared to both. Learning theory and cognitive-behavioral theory are the underpinnings of many successful interventions with persons with dementia. Learning theory has been applied to cases of dementia, demonstrating how best to maximize cognitive abilities, use whatever cognitive strengths remain, and integrate all of this into daily life. Behavioral theory has been applied to the understanding of mood and depressive disorders in those with dementia demonstrating clinical effectiveness in reducing depressive symptoms. Each of these interventions has as its aim to affect the patient's behavior and to improve the psychosocial and physical...

Principle 3 A Correct Diagnosis Is Essential for Providing Accurate Information about Prognosis and Initiating an

The major causes of dementia in the elderly (e.g., Alzheimer's disease, vascular dementia, dementia with Lewy bodies, frontotemporal dementia) have unique causes, clinical features, and natural histories. Despite individual patient differences, there are important similarities in presentation, disease course, and response to treatment in those patients with the same cause of dementia. By making a specific dementia diagnosis, a clinician can better predict a patient's prognosis and expected disease course, better identify atypical variations in the expected disease course that may signify a new problem (e.g., depression or delirium), and better determine which treatments may provide benefit to a patient based on clinical research conducted on patients with a similar, specific dementia diagnosis. In addition, based on Principle 1, it is anticipated that in the future, disease-specific treatments will be effective in those with the disease and ineffective in those without the disease...

Principle 2 Differential Diagnosis Should Always Include Underlying Medical Illnesses Both Minor and Serious Which

Elderly patients are susceptible to delirium, and patients with dementia have an even greater risk of developing delirium with consequent behavioral disturbance, as a result of even minor medical illnesses, such as a urinary tract infection or viral syndrome. In addition, more serious, potentially life-threatening symptoms could have behavioral concomitants in susceptible patients with dementia. For this reason, it is imperative, in the evaluation of such patients, to thoroughly evaluate for comorbid states. Assuming that acute behavioral changes in a dementia patient are only part of the dementia can often delay diagnosis of comorbid states and can lead to unnecessary interventions for behavior.

Principle 4 Psychiatric Symptoms and Hence the Indicated Treatment May Change over the Course of the Patients Illness

Dementia patients, over the course of their illness, may experience various combinations of psychiatric syndromes, so diagnostic approaches and treatment strategies must be flexible to meet patients' needs over time. For example, patients may develop depression early in their illness, with good

Issues In Diagnosis And Treatment

Although AD is the most frequent cause of dementia in affluent societies, vascular dementia and Lewy body dementia are also common in the elderly. Thus, many patients with AD have these comorbid diagnoses. In fact, although Lewy body dementia may occur in pure form, most patients also qualify clinically and neuropathologically for AD. The McKeith criteria for the diagnosis of Lewy body dementia include progressive dementia with coincident parkinsonism, neuroleptic sensitivity, fluctuations in cognition, and spontaneous (not drug-induced) visual hallucinations (McKeith, Galasko, Kosaka, Perry, Dickson, et al., 1996 McKeith, Perry, & Perry, 1999). If indicated, patients may be given a combined diagnosis of AD and Lewy body dementia. This combination is also termed the Lewy body variant of AD. The Hachinski Ischemic Score (HIS Hachinski, Lassen, & Marshall, 1974) as modified by Rosen, Terry, Fuld, Katzman, and Peck (1980) is an autopsy-validated index for the diagnosis of vascular...

Assessing Cognition Mental Status Examinations And Neuropsychological Evaluation

Mental status examination is a major part of the evaluation of cognitive complaint. One of the most commonly used instruments is the Mini-Mental State Examination (MMSE Folstein, Folstein, & McHugh, 1975). The most common clinically useful version is a 30-item structured assessment of memory orientation, concentration, language, and constructional ability. Other screening tests are described briefly in Table 2.1. Among nonminor-ity populations of average education, scores below 27 suggest dementia. When mental status is impaired and there is a reliable informant to confirm functional change, further neuropsychological testing may not be necessary. Table 2.1 Cognitive Screening Measures for Alzheimer's Disease Table 2.1 Cognitive Screening Measures for Alzheimer's Disease dementia high bClock Drawing in Alzheimer's Disease A Novel Measure of Dementia Severity, by T. Sunderland et al., 1989, Journal of the American Geriatric Association, 37, pp. 725-729 and Screening for Alzheimer's...

Assessing Function Evaluation Of Instrumental And Basic Activities Of Daily Living

There are many instruments that capture functional deterioration. However, most are too cumbersome for use in clinical evaluation, and an open, but focused, interview is the usual method for collecting this information. Two domains of function need to be considered instrumental activities of daily living (ADL) and basic ADL. Instrumental ADL refers to the cognitive aspects of function, including the planning of activities to accomplish basic needs. These include activities such as shopping, chores, handling financial matters, and meal preparation. Basic ADL typically refers to eating, grooming, and toileting. Accurate functional assessment usually requires an observant other and usually cannot depend on the patient alone. Because many functional abilities are compromised by aging, it can be difficult to identify functional deficits due to dementia, especially in the earliest stages. Inquiring about subtle changes by asking about how much supervision and physical assistance is needed...

Multicultural Issues In Assessing And Managing Ad

There are a number of multicultural issues in dementia care and the AD patient, including cultural differences in disease presentation and the caregiver experience. Disease presentation may vary according to race. In a large observational study, Shadlen, Larson, Gibbons, McCormick, and Teri Nonpharmacological Approaches to Treating Alzheimer's Disease 35

Environmental Strategiesmodifications

Occupational therapists in ways to simplify the home environment, such as eliminating clutter, breaking down tasks into component parts, and educating the caregiver about dementia and behavioral management. For example, clothing may be laid out according to the order in which it is placed on the body, resulting in reduced anxiety and agitation in patients. A modest effect was seen in patient dependency over time, and caregivers reported improved self-efficacy and reduced disturbance during caregiving activities.

Other Clinical Features of DLB

REM sleep behavior disorder can also be seen in association with DLB (Boeve et al., 1998 Turner, 2002), and some medical literature suggests that the pathologic substrate of idiopathic REM sleep behavior disorder may involve neuronal loss and LBs in the brainstem monoaminergic nuclei important in regulating sleep phenomena. Neuroleptic supersensitivity is another common feature in DLB. It is important to properly recognize DLB because patients with this disorder can be at high risk for developing serious side effects and potentially life-threatening reactions and super-sensitivity to antipsychotic medications. Olfactory function is impaired in a number of neurodegenerative disorders including DLB. A study of olfactory function in 92 patients with dementia and 94 controls with neu-ropathological diagnoses found that subjects with LBs were more likely to be anosmic than those with AD or controls and, among subjects with LBs, overall cortical LB scores and LB density in the cingulate...

Pathologic Anatomic Correlates of Cognitive Behavioral Disturbances in PD

The nature of the histopathologic changes associated with PD with dementia continues to be debated. Although the dementia in PD might be explained by the co-occurrence of AD, mounting evidence argues against this as the sole explanation. in the PD population (allowing for senile plaques only to make a diagnosis of AD Boller, Mizutani, Roessmann, & Gambetti, 1980). Review of other studies reveals a co-occurrence rate of AD to be about 5 to 20 with PD pathology. Furthermore, a study by Hughes, Daniel, and Lees (1993) examining pathologically verified cases of PD revealed that all had cortical Lewy bodies (LB), but not all had a sufficient quantity to be classified as DLB. When these investigators further examined just those PD patients with well-documented dementia (33 ), they found that only one-third had additional pathological changes of coexisting AD. DLB was found in one-tenth, and a vascular cause was seen in one-fifteenth. Thus, half of the well-documented dementia patients...

Epidemiology Prion Diseases

CJD has sporadic, familial (i.e., genetic), and transmissible (i.e., infectious) forms. This section focuses on sporadic and transmissible forms. Genetic forms of prion diseases are discussed in the next section. Sporadic CJD accounts for at least 85 of human prion disease cases. A review of 230 consecutive cases of sporadic CJD revealed that the disease affects men and women approximately equally with a majority of cases occurring between the ages of 55 and 75 years (range 19 to 83 years, average age of onset 61.5 years Brown, Cathala, Castaigne, & Gajdusek, 1986). Cognitive decline was the earliest neurologic symptom in two-thirds of cases however, one-third presented with noncognitive neurologic symptoms such as gait disturbances or, less commonly, changes in vision. Rapidly progressive dementia, myoclonus, extrapyramidal signs, and periodic EEG activity were seen in a majority of cases during their disease course. The mean duration of illness before death was 7.6 months....

Treatment Prion Diseases

Care for patients and support for their families. For example, myoclonus and seizures can be controlled with anticonvulsant medications such as valproic acid and benzodiazepines. Severe hyperkinetic movement disorders such as chorea or dyskinesias and psychotic behavioral symptoms can be controlled with neuroleptic medications. Other psychiatric symptoms can be improved with medications that are used for behavioral symptoms in other patients with dementia. Quality nursing care is very important and can limit pain and the complications of being bedridden. Finally, and most importantly, patients and their families need a tremendous amount of emotional and social support to cope with these devastating diseases.

Diagnostic Standards

Two international conferences on frontotemporal dementia culminated in clinical and neuropathological diagnostic criteria for frontotemporal dementia (Brun et al., 1994), often referred to as the Lund-Manchester criteria in the literature. Using the broad term frontotemporal dementia (FTD), the clinical criteria of FTD include core diagnostic features, which include behavioral disturbances, affective symptoms, speech disturbance, intact spatial orientation and praxis, physical signs, and laboratory tests, including brain imaging and neuropsychological test results. Supportive diagnostic features such as presenile onset and positive family history, as well as diagnostic exclusion features, are also delineated. The consensus group also outlined the neuropathological features that are distinctive of frontal lobe degeneration type, Pick's disease, and MNDD. A subsequent update of the criteria included consensus criteria for progressive nonfluent aphasia and semantic dementia (Neary et...

Symptoms Cognitive Deficits

The differential diagnosis between FTD and affective disorders can be difficult. Symptoms such as lack of concern, withdrawal, lability, impulsiveness, irritability, aspontaneity, poor planning and judgment, and disinhibition can be easily misinterpreted as either unipolar or bipolar mood disorders. One-third to two-thirds of FTD patients referred to specialty dementia clinics were tentatively diagnosed with a psychiatric disturbance by their general physicians (Gregory & Hodges, 1996 Pasquier, Lebert, Lavenu, & Guillaume, 1999). According to Brun and Gustafson (1999), the majority of FTD and Pick's disease patients are initially treated with antidepressant medications. Only a few empirical studies have compared the behavior and mood problems seen in FTD patients to other dementia groups. Behavioral disturbances (personality change, disinhibition, irritability, euphoria, aggression, lability, and changes in oral dietary behavior) were present in all FTD patients but only 19 of...

Evolution Of The Concept Of

In 1910, Emil Kraepelin formulated the initial concept of arteriosclerotic dementia, a denomination that encompassed all cases of dementia in old age (senile dementia) and remained practically unchallenged for the next 60 years. VaD was originally called arteriosclerotic insanity by Otto Binswanger and Alois Alzheimer, who separated VaD from syphilitic dementia paralytica and from other forms of senile and presenile dementia (Mast, Tatemichi, & Mohr, 1995). Alzheimer and Binswanger were the first to underline the large clinicopathological spectrum of VaD. Arteriosclerotic dementia incorrectly became synonymous with senile dementia, and it was widely held that cortical atrophy in the elderly resulted from progressive strangulation of blood flow leading to hypoxic neuronal death. This idea prevailed until 1974 when Hachinski, Lassen, and Marshall proposed the name multiinfarct dementia (MID), based on the findings of Tomlinson, Blessed, and Roth (1970), who were able to correlate...

The Nindsairen Criteria

Dementia, that is, impairment of memory and two other cognitive domains, such as executive function, attention, or orientation. The deficit should be severe enough to interfere with activities of daily living and not be explained solely by the motor consequences of the stroke. 3. A link between dementia and vascular lesions, usually defined by onset of dementia within three months following a stroke. However, Binswanger's disease and lacunar state resulting from multiple lacunes two types of VaD associated with small vessel disease may present as a slowly progressive subcortical-type dementia syndrome. Onset of the disease in these patients is often difficult to determine. In these two instances, the link between imaging and dementia is provided not by a temporal link but by the location and extent of the lesions.

Separating Ad From

The Nun Study (Snowdon et al., 1997) reported that in very old subjects, lacunes are an important factor in the clinical expression of AD. The difficulties in separating VaD from AD have been stressed, and the names mixed dementia or AD plus CVD have been used for cases combining vascular and degenerative pathologies. In addition, patients with anterior choroidal artery stroke may fulfill criteria for AD (Sarangi et al., 2000). As mentioned before, the prevalence of cerebrovascular and cardiovascular diseases increases steeply with age therefore, histological changes of AD in the elderly often coexist with stroke and vascular pathology (Galasko et al., 1994 Lim et al., 1999). Lacunar strokes appear to multiply the effect of AD lesions, whereby, in elderly subjects with presence of one or two lacunar strokes, the likelihood of clinically manifesting a dementia is increased 20-fold (Snowdon et al., 1997). Also, a lesser amount of senile plaques and neurofibrillary tangles are required...

Frontal Executive Function

VaD is characterized clinically by executive dysfunction, that is, the prominent loss of executive function (Cummings, 1994). This is a major component of the cognitive disability and the dementia and explains the loss of planning capacity, working memory, attention and concentration, stimuli discrimination, abstraction, conceptual flexibility, and self-control (Fuster, 2000 Royall et al., 2002). Frontal executive functions control volition, planning, programming, and monitoring of complex goal-directed activities such as cooking, dressing, shopping, and housework. Patients with executive dysfunction are often capable of performing individual steps of a complex problem but are unable to provide a correct strategy to solve it. In contrast with AD, memory loss is not an early feature of VaD and is never as profound as in AD. Tests for instrumental activities of daily living are a good surrogate of executive function control.

Public Health Aspects Of

Of major public health interest are the results of treatment trials of hypertension and use of statins in the elderly showing decreased incidence of dementia. Treatment of other risk factors for VaD is also indicated, including smoking, hyperfibrinogenemia, orthostatic hypotension, cardiac arrhythmias, congestive heart failure, and obstructive sleep apnea. Blood glucose control in patients with diabetes and lowering of fibrinogen and lipids should be beneficial. Food supplementation with folic acid has been recently implemented in an effort to reduce effects of hyperhomocysteine-mia on vascular disease. Other preventable factors should be determined in an effort to decrease the risk of dementia and disabling stroke with appropriate preventive treatment (Rom n, 2002b).

Clinical Diagnosis

Despite the apparent inaccuracy of clinical diagnosis of MD, as reviewed later, it is important to examine how the clinical diagnosis of MD is most often reached. The Hachinski Ischemia Scale (HIS), originally developed to diagnose VaD, has also been used to classify MD. The presence of dementia and low scores on this scale (4 or lower) are classified as AD and high scores (7 or higher) as VaD (Hachinski et al., 1975). However, the validity of using intermediate scores from this scale to diagnose MD has been questioned by neuropathological studies. Only 18 of verified MD cases had HIS scores Clinical diagnosis is often made based on medical history, physical examination, brief rating scales such as the MMSE and the Blessed Dementia Rating Scale, full neuropsychological batteries, blood tests, and neuroimag-ing results. The value of adding the more expensive procedures, that is, neuropsychological tests, blood work, and neuroimaging tests was examined (Chui & Zhang, 1997). Customary...

Mood and Behavioral Disturbances

Overall, the behavioral and psychological symptoms of dementia are such a salient feature of the disease that there is now a push to include this as a diagnosis or syndrome in the International Classification of Diseases (ICD Zaudig, 2000). Depression and anxiety are common in dementia, and these can be the first symptoms of a dementia in the absence of initial cognitive deficits (Reding, Haycox, & Blass, 1985). The clinician should suspect a mood or anxiety disorder in individuals presenting with possible dementia, most particularly in persons who are aware of their memory and cognitive failings, compared to patients whose relative or caregiver is noticing the cognitive difficulties (U.S. Department of Health and Human Services, 1996). An individual in the early stages of dementia is more likely to experience a mood or anxiety disorder than one in the moderate or later stage (Merriam, Aronson, Gaston, Wey, & Katz, 1988). The clinical interview is a necessity in ruling out a...

Pathophysiology Infectious

The pathogen in HIV dementia is the RNA retrovirus itself. HIV penetrates the CNS at or near the time of seroconversion, likely through infected mononuclear cells. Productive infection occurs much later, when the host is immunosuppressed (McArthur, 2000). The pathologic hallmark of HIV infection is the multinucleated giant cell. The periphery of this cell is ringed with nuclei and has vacuolated cytoplasm. The multinucleated giant cell contains HIV nucleic acids and may reflect viral replication. Other pathologic findings include perivascular inflammatory infiltrates and microglial nodules. The latter contain microglia, macrophages, and lymphocytes. Both multinucleated giant cells and microglial nodules are widely distributed in the brain but are more apparent in white matter, basal ganglia, and thalamus (Budka, 1991). White matter often demonstrates diffuse pallor. Cortical atrophy, gliosis, and neuronal loss are observed with a frontotemporal predisposition. Surviving neurons have...

Epidemiology And Prevalence

Hallucinations are also common in dementia, with a prevalence between 21 and 49 in different studies (Burns et al., 1990 Mega et al., 1996). Visual and auditory hallucinations are most common. Varying degrees of agitation occur in one-third to one-half of AD patients (Cohen-Mansfield, Marx, & Rosenthal, 1989 Devanand et al., 1997), with aggressive behavior being less common (Swearer, Drachman, O'Donnell, & Mitchell, 1988). The large ranges in prevalence rates may be explained, in part, by the various settings where the information was gathered (e.g., outpatient, assisted living, nursing home) and differing methods of assessment. Delusions are most prevalent during the middle phase of illness (Cummings et al., 1987 Mega et al., 1996 Wragg & Jeste, 1989) and are a common precipitant of institutionalization (Stern et al., 1997). The informant (e.g., direct clinical interview with the patient, interview with the caregiver, or chart review), criteria for diagnosis of...

Clinical Characteristics in Psychosis of AD

Psychotic signs associated with dementia include delusions, hallucinations, and misperceptions. As noted previously, the vast majority of patients with dementia are likely to develop psychosis, agitation, aggression, or disruptive behavior over the course of their illness. There have been many attempts to biologically and psychologically link psychotic symptoms to agitation and aggression. In schizophrenia, antipsychotics are often assumed to be specific for the treatment of psychosis, and improvement in symptoms of behavioral dyscontrol is believed to be secondary to improvement in psychosis. Unfortunately, this close association in schizophrenia does not appear to apply to patients with dementia. In fact, in a doubleblind placebo-controlled trial that compared risperidone, haloperidol, and placebo, there were no differences among active medications for psychosis (both were effective), but aggression was reduced both in severity and frequency to a greater extent on risperidone...

Location of Patient Being Treated

The location of the patient (nursing home, assisted living, or outpatient) does not alter the choice or dose of medication to be considered in treating psychotic symptoms in dementia. The residential status of a patient is partly dependent on the patient's clinical state and partly on the ability of the caregiver to manage the patient at home. Whether and when the patient is admitted to a nursing home are highly variable factors that may depend as much on the caregiver's tolerance threshold and available resources as the patient's clinical state. Furthermore, the range of semi-independent, assisted living, intermediate nursing care, and specialized dementia facilities has created a spectrum of caregiving that defies simple categorizations and overlaps with intensive in-home services. In both outpatients and nursing home patients, the results of trials comparing antipsychotic medications in AD (De Deyn et al., 1999) and dose-comparison studies of individual antipsychotic medications...

Current Treatment Conventional Antipsychotics

Placebo-controlled trials of antipsychotics in dementia have been conducted and published. Most studies were conducted in inpatient units or in nursing homes. In a four-week trial, thiothixene (< 15 mg day) demonstrated marginal superiority over placebo in the treatment of 42 patients with organic brain syndrome (Rada & Kellner, 1976). Limited information about diagnosis, nonstratified assignment of psychotic patients to the treatment groups, short trial duration, and a high placebo response rate (55 ) were problematic. In another study of 61 patients with dementia (30 AD and 26 vascular), global clinical improvement was significantly greater with haloperidol (35 , mean daily dose 4.6 mg) or loxapine (32 , mean daily dose 21.9 mg) compared to placebo (9 ). A large proportion had vascular dementia (42.6 ), and the use of antiparkinsonian agents and chloral hydrate were limitations (Petrie et al., 1982). In another study of 53 patients, loxapine and thioridazine showed a small...

Comparisons among Conventional Antipsychotics

Earlier studies comparing low-potency to high-potency antipsychotics did not show consistent differences in efficacy (Barnes et al., 1982 Carlyle et al., 1993 Cowley & Glen, 1979 Petrie et al., 1982 Rosen, 1979 Smith, Taylor, & Linkous, 1974 Tsuang, Lu, Stotsky, & Cole, 1971). These studies were often limited by the lack of a placebo control and diagnostic heterogeneity in sample selection. Overall, there is little evidence to indicate superior efficacy for a specific class of conventional antipsychotic in the treatment of neuropsychiatric disturbances in dementia (Devanand, 1995 Salzman, 1987).

Choice of Conventional versus Atypical Antipsychotic

The propensity for conventional antipsychotics to cause EPS in dementia and to increase the risk of tardive dyskinesia in elderly psychotic patients (Jeste, Lacro, et al., 1999) has led to a growing preference for atypical anti-psychotics in the treatment of patients with dementia who develop psychosis or behavioral dyscontrol. However, it is important to note that there is no evidence of superior efficacy for any atypical antipsychotic compared to any conventional antipsychotic in the treatment of psychosis in dementia. In the only controlled treatment trial comparing an atypical antipsychotic to a conventional antipsychotic, De Deyn et al. (1999) compared the effects of risperidone, haloperidol, and placebo in a double-blind placebo-controlled flexible-dose study for behavioral dysregulation of dementia (not psychosis of dementia). They used a 30 reduction from baseline to endpoint in BEHAVE-AD total score as responder criteria. They found in 344 patients with dementia and...

Importance Of Diagnosis And Treatment

Once a diagnosis of dementia is established, the clinical picture often remains complex. The diagnosis of depression in dementia is made challenging by overlap symptoms common to the two disorders. Communication difficulties in later stages of dementia as well as increasing reliance on caregiver reports may also increase the difficulty of diagnosis of depression (Thorpe & Groulx, 2001). However, although difficult, accurate diagnosis of depression in dementia is of clinical importance. Diagnosis and treatment of depression is worthwhile in any individual in an attempt to alleviate individual suffering. Additional multiple other benefits of treatment of depression in dementia are possible and include removal of any depressive contribution to memory problems, improving functional status, potential cost savings of excess health care utilization due to depression, and reducing caregiver burden.