Cure Dementia Naturally

Super Memory Formula

After the harsh reality that the doctor had to face his son ending his life, he suffered a major irreversible memory loss disease. This caused him to fall into depression and depend on the drugs from the pharma which was devasting for his mental and physical health and on so many other levels. After countless hours of research and experimentation, he realized that the root of all problems of memory loss was an enzyme that eats away the memory cells when the person gets older. This makes the person forget their loved ones, family and friends as if they have never met them. In some cases, they even forget about their past experiences, if they had children, how they came to the place they are in right now and who they are in the first place. This was exactly what the doctor had in his future if he did not make a decision. But he did and met with great people who helped him find the cure. This was a groundbreaking study that no one wanted to believe or endorse because it would go against the large pharma industry. However, the information is in there to protect yourself and your loved ones from such a devastating experience. You only need to follow the link and you will be guided to get the information downloaded to your device and follow the all-natural ways to get rid of memory loss. Read more...

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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...

Natural Models Of Alzheimerlike Pathology

Cerebral amyloid deposition was first noted in a nonhuman species in the 1950s by von Braunmuhl, who described senile plaques in elderly dogs. Since then, the characteristics of the deposits and the natural history of their emergence have been well established, as has their possible relationship to age-associated cognitive decline. In dogs, as in primates, the A peptide is identical in sequence to human A . Normal rats and mice differ in three amino acids from humans. The deposits that arise in the parenchyma of the aged canine brain are usually diffuse in nature i.e., fully developed, dense-cored senile plaques are relatively rare. However, cerebral amyloid angiopathy (CAA) is common in older dogs (Wegiel et al., 1995). CAA in canines, as in humans, primates, and transgenic mice, is associated with an increased incidence Af3 accumulation correlates with behavioral impairments in aged dogs (Colle et al., 2000), and with a regional loss of brain substance (particularly in the frontal...

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.

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.

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

(PPND), familial multiple system tauopathy with presenile dementia (FMST), hereditary dysphasic disinhibition dementia (HDDD), and familial progressive subcortical gliosis (FPSG). Common clinical manifestations of these families were changes in behavior including apathy, disinhibition, repetitive behavior, and loss of personal awareness and cognition including early impairment of executive cognitive function with relative preservation of memory, orientation, and visuospatial function. Motor features such as parkinsonism, dystonia, upper and lower motor neuron signs (i.e., spasticity and amyotrophy), and oculomotor disturbances were common during the course of disease. Review of autopsy material from these families demonstrated that frontotemporal atrophy, neuronal or glial tau inclusions, and ballooned cells (Pick cells) were seen in most, but not all, families. The consensus conference recommended these and other families linked to this region be named frontotemporal dementia and...

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...

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...

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

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...

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...

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,...

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 The most widely accepted criteria for LBD (McKeith et al., 1996) are progressive cognitive decline and two of the following fluctuating cognition 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...

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...

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...

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...

Rat Models of Age Related Cognitive Decline

Naturally occurring rat models can be useful for studying age-related cognitive decline. Long-Evans rats trained on the Morris water maze have been used to model individual differences in cognitive abilities that depend on the medial temporal lobe system. This approach has yielded a great deal of new information including the unexpected lack of neuronal loss in the hippocampus in aged rats with pronounced cognitive impairment. Despite this absence of neuron death, aged rats with impaired memory can be distinguished from those with intact memory at the neurobiological level. Cellular and molecular changes include alterations in the electrophysiological properties involved in synaptic plasticity, alterations in gene and protein expression, and efficacy of cell signaling pathways. The prefrontal cortex and cognitive abilities supported by this brain region are also subject to age-related decline. The rat prefrontal cortex performs certain aspects of what is conventionally known as...

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).

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...

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...

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...

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.

Comparability To Human Agerelated Cognitive Decline

There is substantial evidence that specific factors that adversely impact cognition in rat models also correlate with age-related cognitive impairment in primates, including humans. For example, assessment of the degree of atrophy of the medial temporal lobe in humans is an effective predictor for the development of dementia in patients with mild cognitive impairment (Korf et al., 2004), and medial temporal lobe atrophy in stroke patients predicts poor cognitive performance (Jokinen et al., 2004). Likewise, lesions of medial temporal lobe structures induce memory impairments in rodents (reviewed by Jarrard, 1993). Moreover, age-related changes such as alterations in the glucocorticoid system and increases in oxidative stress are found among aged rat and human populations (Bizon et al., 2001 Nicolle et al., 2001 de Quervain et al., 1998 Roozendaal, 2002 de Quervain et al., 2003 Lupien et al., 2005). Finally, as discussed in more detail below, the absence of frank neural loss among aged...

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.

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).

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...

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

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.

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...

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...

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...

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...

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...

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).

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,...

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)...

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).

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...

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.

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...

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...

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.

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...

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.

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.

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...

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,...

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,...

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...

Alzheimers Disease

Refolding or misfolding of another protein endogenous to human brain tissue, P-amyloid, is also a prominent feature of Alzheimer's disease. While the root cause of Alzheimer's disease remains elusive, the characteristic senile plaques and neurofibrillary bundles contain aggregates of the protein P-amyloid, a 4.3-kDa polypeptide produced by proteolytic cleavage of a larger protein known as amyloid precursor protein. In Alzheimer's disease patients, levels of P-amyloid become elevated, and this protein undergoes a conformational transformation from a soluble a helix-rich state to a state rich in P sheet and prone to self-aggregation. Apolipopro-tein E has been implicated as a potential mediator of this conformational transformation.

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...

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...


Dementia is not a specific disorder or disease. It is a syndrome (group of symptoms) associated with a progressive loss of memory and other intellectual functions that is serious enough to interfere with performing the tasks of daily life. Dementia can occur to anyone at any age from an injury or from oxygen deprivation, although it is most commonly associated with aging. It is the leading cause of institutionalization of older adults. The definition of dementia has become more inclusive over the past several decades. Whereas earlier descriptions of dementia emphasized memory loss, the last three editions of the professional's diagnostic handbook, Diagnostic and Statistical Manual of Mental Disorders (also known as the DSM) define dementia as an overall decline in intellectual function, including difficulties with language, simple calculations, planning and judgment, and motor (muscular movement) skills as well as loss of memory. Although dementia is not caused by aging itself most...

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).

Poststroke dementia

Post-stroke dementia (PSD) is currently defined as any dementia occurring after stroke. The overall statistic is striking as the incidence of stroke doubles the risk of dementia. There is also a direct link between stroke and development of Alzheimer's disease although the latter is responsible only for part of the eventually developed dementias the fraction of patients with Alzheimer's disease accounts for 20-60 per cent of those with PSD. A particular type of post-stroke dementia is represented by Binswanger's disease, (or subcortical dementia), which is a form of vascular dementia characterized by diffuse white matter lesions it leads to progressive loss of memory, cognition and behavioural adaptation. The infarct occurring in white matter triggers progressive death of oligodendrocytes, activation of microglia and degeneration of axons. The primary pathological steps most likely are associated with ischaemic death of oligodendrocytes.

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). Normal pressure hydrocephalus (gait disorder, urinary incontinence and cognitive decline). Creutzfeld-Jakob disease (rare, rapid decline, myoclonus though this can be seen in other dementias ). Treatable causes of dementia include

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...

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...

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.

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.

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.

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...

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...

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.

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...

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.

Diagnostic Standards

Diagnosis of MD is inherently linked to diagnostic criteria for AD and VaD. The National Institute of Neurologic Communicative Disorders and Stroke-Alzheimer Disease and Related Disorders Association (NINDS-ADRDA) established a consensus for the neuropathological diagnosis of AD by quantifying the neuritic or senile plaques in a given anatomical region for specific age groups. However, such consensus for the diagnosis of VaD does not exist. Thus, much of the confusion in the definition of MD and, therefore, prevalence rates of MD stems from the evolving, yet unresolved, definition of VaD. Two widely recognized diagnostic standards for VaD and MD have been established, one by NINDS-AIREN and the other by the State of California ADDTC. The NINDS-AIREN diagnostic criteria recommend that the term mixed dementia be discouraged from epidemiological studies because the vascular contribution to the dementia is ill defined, whereas the role of neuronal depopulation is clear (Rom n et al.,...

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...

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.

Impact on Functional Status

Depression in dementia is known to cause reduction in functional status at any stage of dementia. Pearson, Teri, Reifler, and Raskind (1989) demonstrated that patients with Mini-Mental State Scores (Folstein, Folstein, & McHugh, 1975) of 16 to 19 were unable to perform instrumental activities of daily living (IADLs) in the presence of depression, whereas those at the same cognitive level without depression could do so. A later study extended this finding, reporting that the presence of depression was predictive of functional status in AD, with mildly cognitively impaired subjects less able to perform IADLs and moderately cognitively impaired subjects less able to perform activities of daily living (ADLs Fitz & Teri, 1994). Hargrave, Reed, and Mungas (2000) also found a link between depression in dementia and functional impairment. This diminished function as well as aggression (Lyketsos et al., 1999) and other behavioral difficulties such as vocal disruption (Dwyer & Byrne,...

Pathophysiology Neurotransmitter Abnormalities

Several groups have hypothesized a neurological basis for depression in AD in the locus ceruleus (Forstl et al., 1992 Zubenko & Mossy, 1988 Zweig et al., 1988). These studies reported that the antemortem development of depression in patients with AD was found to be associated with degenerative changes in the locus ceruleus, substantia nigra, dorsal raphe, and basal nucleus of Meynert on autopsy. However, a more recent study (Hoogendijk et al., 1999) refuted these earlier results, finding no supplementary loss of pigmented neurons in the locus ceruleus in patients with depression and AD. These authors suggested that the findings of the earlier studies may be explained by the fact that patients with depression in AD in those studies may have been at more advanced stages of dementia.

Neuroendocrine Theories

Hypercortisolemia associated with late-life depression has been found to be associated with neuronal degeneration in the rat as well as human hippocampus (Sapolsky, 2000 Sheline, Wang, Gado, Csernansky, & Vannier, 1996). Thus, a neuroendocrine hypothesis for depression as a risk factor for dementia holds that late-life depression-induced cortisolemia could cause hippocampal degeneration and eventual cognitive decline. Lupien et al. (1994) found that aged subjects showing significantly increased cortisol levels with age and with high basal cortisol levels had impaired cognitive performance compared to aged controls without those abnormalities. Katona and Aldridge (1985) found failure of suppression on the Dexam-ethasone Suppression Test (DST) in 10 of 20 patients with dementia non-suppressors had significantly higher depression scores on the Depressive Signs Scale (DSS) than suppressors. Following antidepressant treatment, three of eight nonsuppressors reverted to normal...

The Question of Symptom Persistence

Some have suggested that many depressive symptoms are largely transient, mild, shallower, or self-limited in patients with dementia (Devanand et al., 1997 Katz, 1998). O'Connor, Pollitt, and Roth (1990) and Forsell, Jorm, and Winblad (1994) found remissions of depression in all of their subjects with depression in dementia at baseline. However, other studies have found evidence for the persistence of depressive symptoms syndromes. Janzing, Teunisse, and Bouwens (2000) reported that both syndromal and subsyn-dromal depression were highly persistent in nursing home residents with dementia, few of whom were treated with antidepressants. Another study demonstrated a recurrence rate of 85 for depressive symptoms in dementia (Levy et al., 1996). In terms of major depression, there is evidence for a chronic course of depression in dementia, with one study reporting that 58 of subjects with major depression in dementia still had depression at 16-month follow-up (Starkstein et al., 1997).

Cholinesterase Inhibitors

There is a paucity of data as to the effect of cognitive enhancers on depression in dementia. There is some suggestion that these medications may reduce anxiety and apathy in AD patients (Levy, Cummings, & Kahn-Rose, 1999), leading to conjecture that these medications could be ameliorating subsyndromal depression in some cases. Kaufer, Cummings, and Christine (1996) conducted an open-label study of tacrine on behavioral symptoms

Nonpharmacological Treatments Electroconvulsive Therapy ECT

The data on ECT and depression in dementia are limited. However, among patients with severe or medication-refractory depression, ECT should be considered. Limited data suggest that the outcome may be similar to elderly patients without dementia, however, with increased post-ECT confusion likely in patients with dementia (Nelson & Rosenberg, 1991). A retrospective study of ECT in depressed elderly patients with AD, VaD, or other types of dementia found significant discharge improvements in both mood and cognition, although 49 of patients developed a delirium during the ECT course (Rao & Lyketsos, 2000a). The authors of this study suggest that the confusion seen during ECT could be minimized by decreasing the frequency of treatment to one to two times per week.

Interpersonal Behavioral Approaches

As noted in Table 10.3, significant placebo response has been found in three of the four placebo-controlled trials. Katz (1998) noted that the pronounced improvement of depressive symptoms in placebo groups in those trials suggests that interpersonal or behavioral approaches might be effective in the treatment of depression in dementia. Teri, Logsdon, Uomoto, and McCurry (1997) studied two types of behavioral interventions the use of pleasant events for patients living in the community and teaching problem solving for their caregivers compared to a control wait-list condition in depressed patients with AD. Both approaches were associated with significant improvement in depressive symptoms in both patients and caregivers, and the improvement was maintained for six months. These results suggest that

Depression As Prodrome Or Risk Factor

In conceptualizing depression as a prodrome for dementia, specifically for AD, depression is expressly viewed as an early expression of the underlying pathobiology of dementia. This is an important concept in AD because of the general knowledge that there is underlying pathology involved in Alzheimer's many years before symptoms are present and a full-blown clinical dementia syndrome is apparent (Bondi, Salmon, Galasko, Thomas, & Thal, 1999 Morris et al., 2001). There is great interest, therefore, in discovering dementia at its earliest stage of onset so that treatment can postpone and or prevent symptoms. Alexopoulos, Myers, Young, Mattis, and Kakuma (1993) and De-vanand, Sano, and Tang (1996) presented data that could be used to support the prodrome idea. Alexopoulos and colleagues compared two groups of older depressives. One group had cognitive impairment (n 23) that was reversible once antidepressant treatment was completed. The second group was also treated for depression but...

Vascular Depression Hypothesis

A conceptual framework for understanding the mechanisms at work with depression as a prodrome or risk factor for dementia may be the vascular depression hypothesis (Alexopoulos, Meyers, Young, Campbell, et al., 1997 Alexopoulos, Meyers, Young, Kakuma, et al., 1997). This hypothesis states that vascular risk factors and or disease can predispose, precipitate, or perpetuate depressive disorders in older age. The authors speculate that specific disruption of the frontal-subcortical brain circuitry is responsible for the mood disorder. O'Brien et al. (1996) investigated white matter changes in a group of normal adults age 55 years and older (n 40), depressives age 55 years and older (n 61), and a group of nondepressed Alzheimer's patients (n 68). The authors confirmed Coffey's finding that white matter changes were common in 59 of normal elders. White matter changes were extremely common in depressives, with 85 having these changes and 30 showing severe changes. Overall, deep white matter...

Clinician Rating Scales

Clinician rating scales are typically completed after interactions with persons with dementia, with family and or professional caregivers, and after clinician observation of behavior. In many ways, then, these assessments may be the most complete and objective. Limitations of these scales, however, include Statements and views of the person with dementia are always overridden by caregiver report. The two most commonly used rating scales are the Hamilton and the Cornell scales. We include a brief description of those, along with the Consortium to Establish a Registry for Alzheimer's Disease (CERAD) scale, which taps into a more focused domain of affective functioning. The Hamilton Rating Scale for Depression (HRSD Hamilton, 1967), the gold standard in most outcome research on depression in dementia, has been used the longest with older persons with dementia. Several versions of the HRSD have been used. The most common version is a 17-item scale on which each item is rated on a three-...

Self Report Measures Geriatric Depression Scale GDS

While there are many self-report depression measures that have been used with older adults (e.g., CES-D, Zung, Beck), the Geriatric Depression Scale is by far the one with the most applicability to older persons with dementia. Historically, the usefulness of the GDS has been called into question. Burke, Houston, Boust, and Roccaforte (1989) and Kafonek et al. (1989) reported that the clinical utility of the GDS was poor in long-term care residents with dementia. Lesher and Berryhill (1994) and Parmelee, Katz, and Lawton (1989) provided evidence that the GDS was both internally consistent and clinically valid in individuals with mild to moderate dementia. Two more recent studies have provided further support for the importance and validity of using the report of persons with dementia in any evaluation of mood. In a study mentioned earlier (Espiritu et al., 2001), dementia patients' self-report of depression was a unique and significant predictor of the caregiver reports of patients'...

Conventional Antipsychotics

Evidence from two meta-analytical studies of conventional antipsychotics illustrates that the effects of these agents were consistent and modest, that no single agent showed superiority, and that side effects tended to emerge in a predictable fashion and ultimately define selection of a particular agent. Both reviews examined the use of conventional antipsychotics for behavioral disturbance rather than for specific symptoms or psychoses. Schneider, Pollock, and Lyness (1990) reported the overall result that 59 of patients treated with a conventional antipsychotic showed categorical behavioral improvement versus 41 of those receiving placebo, an 18 drug-placebo difference. This difference is referred to as the effect size, that is, an objective measure of actual drug effect that factors in the effect of placebo. Remarkably, the figure of 18 tends to stand up across trials of most psychotropic agents conducted since that time, as becomes evident in this review. Placebo response rates in...

Summary of Atypical Antipsychotics

The atypical antipsychotics as a class are very likely better tolerated than typical antipsychotics and at least as efficacious. Within the class of atypi-cals, there appear to be modest differences in terms of clinical effectiveness, but the significance of these differences is unclear. There are limited long-term data addressing either safety or efficacy of these agents in the elderly and even less in people with dementia. Jeste, Okamoto, Napolitano, Kane, and Martinez (2000) reported a cumulative incidence rate for tardive dyskinesia of 2.6 in 330 patients with dementia treated openly with risperidone (mean dose of about 1 mg day) for a median of 273 days. This figure is considerably less than that reported in older subjects treated with conventional agents (Jeste et al., 1995) and is consistent with data reported in a prospective longitudinal study of risperidone and haloperidol in older subjects with mixed psychiatric disorders (Jeste et al., 1999). We are not aware of long-term...

Risk Factors Comorbidity

The risk for developing dementia is age related and increases substantially after the age of 75 years. Persons in this age range commonly suffer from a number of chronic conditions, which can exacerbate the behavioral symptoms associated with dementia. The treatment of choice for the behavioral symptoms of dementia has long been the use of psychotropic medications (L. S. Schneider, 1993). However, many patients do not respond favorably to such treatment (L. S. Schneider, Pollock, & Lyness, 1990). For example, Cariaga, Burgio, Flynn, and Martin (1991) found that medication is not effective in decreasing disruptive vocalizations without heavily sedating the patient, thus restricting the general behavioral repertoire of the persons with dementia. Further complicating the use of psychopharmacology with older adults is the fact that many are already taking multiple medications to manage other physical illnesses, making drug-drug interaction effects more likely in this population.

Personality Characteristics

A few studies have examined linkages between premorbid personality traits and problematic behaviors in persons with dementia. Kolanowski, Strand, and Whall (1997) found a highly significant correlation between premorbid neuroticism and aggression in persons with dementia. Magai, Cohen, Culver, Gomberg, and Makatestsm (1997) found evidence that premorbid personality characteristics linked to emotionality show stability of expression across mid- to late-stage dementia. For example, premorbid attachment style predicted current degree of positive affect expressed by nursing home residents with dementia. Premorbid levels of hostility were associated with residents' levels of anger, contempt, and disgust. Their findings also suggested that high levels of premorbid hostility might put nursing home residents at risk for developing depression. This linkage between hostility and depression in persons with dementia is echoed in Menon et al.'s (2001) finding that nursing home residents with...

Nonpharmacological Treatments Focus on Unmet Needs

In some cases, behavior problems may be a manifestation of unmet needs of the person with dementia (Cohen-Mansfield, 2001 Crose, 2000 Richards et al., 2000). Many individuals, particularly in advanced stages of dementia, are unable to convey basic needs such as hunger, thirst, or need for toileting, much less the need for companionship or affection. Further, for some individuals, a need for independence or autonomy may be expressed as aggressive or agitated behavior. Finally, individuals who exhibit problem behaviors may be suffering from either a lack or an excess of environmental stimulation. Because the person with dementia may not be able to communicate his or her needs in traditional ways, caregivers must attempt to determine whether a need is not being met. Subsequently, caregivers must exercise patience and persistence in an often-frustrating, trial and error attempt to determine the root of the individual's behavior problem. If an individual is expressing a less tangible need...

Communication Problems

Communicating with persons with dementia is often challenging as expressive and receptive communication skills decline over the course of dementing illnesses. Interventions in this area focus on caregiver training and or enhancing the abilities of persons with dementia. Several programs to enhance caregivers' communication skills with persons with dementia have been developed (e.g., Bourgeois, 1992a, 1992b, 1997 Clark, 1997 Orange & Colton-Hudson, 1998 Orange, Ryan, Meredith, & MacLean, 1995 Richter, Roberto, & Bottenberg, 1995 Ripich, 1994 Ripich, Kercher, Wykle, Sloan, & Ziol, 1998 Ripich & Wykle, 1996 Ripich, Wykle, & Niles, 1995 Tomoeda & Bayles, 1990). Most involve educating caregivers about changes in communication abilities that accompany dementia. As part of this education process, caregivers are shown how previous communication styles must be adapted and new ways of communication must be developed to communicate more effectively with the individual with...

All About Alzheimers

All About Alzheimers

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