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Dementiaa IntrodWhat is Dementia ?uction Dementia is an organic brain syndrome which results in global cognitive impairments. Dementia can occur as a result of a variety of neurological diseases. Some of the more well known dementing diseases include Alzheimers disease (AD), multi-infarct dementia (MID), and Huntingtons disease (HD). Throughout this essay the emphasis will be placed on AD (also known as dementia of the Alzheimers type, and primary degenerative dementia), because statistically it is the most significant dementing disease occurring in over 50% of demented patients (see epidemiology). The clinical picture in dementia is very similar to delirium, except for the course. Delirium is an acute transitory disorder. By contrast Dementia is a long term progressive disorder (with the exception of the reversible dementias).
The course of AD can range anywhere from 1.5 to 15 years with an average of about 8.1 years (Terry , 1988). AD is usually divided into three stages mild, moderate, and severe. Throughout these stages a specific sequence of cognitive deterioration is observed (Lezak, 1993). The mild stage begins with memory, attention, speed dependent activities, and abstract reasoning dysfunction. Also mild language impairments begin to surface.
In the moderate stage, language deficits such as aphasia and apraxia become prominent. Dysfluency, paraphasias, and bizzare word combinations are common midstage speech defects. In the severe stage the patient is gradually reduced to a vegetative state. Speech becomes nonfluent, repetitive, and largely non-communicative. Auditory comprehension is exceedingly limited, with many patients displaying partial or complete mutism.
Late in the course of the disease many neuropsychological functions can no longer be measured. Also primitive reflexes such as grasp and suck emerge. Death usually results from a disease such as pneumonia which overwhelms the limited vegetative functions of the patient. According to the Encyclopedia of Neuroscience dementia is defined as a sustained, multidimensional loss of cognitive function secondary to organic central nervous system damage, unaccompanied by evidence of an acute superimposed state of clouded consciousness as occurs with delirium or reduced arousal. Dementia is not a disease but rather a symptom of many conditions causing brain dysfunction.
It arises as a result of severe and diffuse brain damage. The essential feature of dementia is an intellectual decline resulting from a progressive deterioration in brain functioning. Dementia can occur as a result of a variety of neurological diseases. These include: Alzheimers disease (dementia of the Alzheimer type), cerebrovascular disease in particular Multi-infract dementia (vascular dementia), alcohol related diseases such as Marchiafava-Bignami disease (alcoholic dementia), AIDS (AIDS dementia complex), Creutzfeldt-Jakob disease (myoclonic dementia), Picks disease, Huntingtons disease, Parkinsons disease, normal pressure hydrocephalus (NPH), and progressive supranuclear palsy (PSP). Dementia is commonly differentiated along two dimensions: age and cortical level. The first dimension, age, distinguishes between senile and presenile dementia.
Senile dementia is used to describe patients who become demented after the age of 65, whereas presenile dementia applies to patients who become demented prior to that age. Late onset AD (LOAD)Alzheimers disease also known as senile dementia Alzheimers type (SDAT) is the predominant cause of senile dementia. Early onset AD (EOAD)lzheimers disease is the most frequent cause of presenile dementia,; but HDuntingtons disease, Picks disease and Creutzfeldt-Jakob disease though not as frequent are also important causes in presenile dementia. The second dimension, cortical level, differentiates between cortical and subcortical dementia. Cortical dementia is used to describe dementia which results from brain lesions at the cortical level, whereas subcortical dementia describes dementia resulting from subcortical brain lesions.
ADlzheimers disease (AD) and Picks disease are the best known examples of cortical dementia; whereas HD, Parkinsons disease (PD),ntia; while Huntingtons disease (HD), Parkinsons disease (PD), and progressive supranuclear palsy (PSP)PSP are good examples of subcortical dementia (Mayke, 1994). Dementia with both cortical and subcortical features is also possible, in that case the term mixed dementia is used. Multi-infract dementiaID is a common example of mixed dementia. Historical developments in dementia Pre-Modern Developments The use of the term dementia dates back to Roman times. The Latin word dementia, derived from the Latin demens , did not originally have the specific connotation that it does today.
It meant being out of ones mind and, as such, was a general term for insanity or insanitymadness (Pitt, 1987). It was the encylopedist Celsus who first used the word dementia in his De re medicina,, published around AD 30. A century later the Cappadocian physician Aretaeus first describeds senile dementia with the word dotage (i.e., The dotage which is the calamity of old agedotage commencing with old age never intermits, but accompanies the patient until death.). Curiously, dementia was mentioned in most systems of psychiatric classification throughout pre-modern times, though the precise meaning of the word is often unclear In the Dark and Middle Ages, through the Renaissance, and well into the 18th century, dementia is mentioned in most systems of psychiatric classification, though the precise meaning of the word is often unclear(Pitt, 1987). Nineteenth Century It can be argued that the origins of the scientific study of dementia date back to the early nineteenth century.
The initial steps were undertaken by the great French psychiatrist Pinel at the beginning of that century. Pinels observations led him to the conclusion that the term dementia should be applied in relation to the progressive mental changes seen in some idiots (Pitt,3). Furthermore, Pinel thought that dementia was a distinct abnormal entity, and thus he used the term dementia to designate one of the five classes of mental derangement. The father of modern psychiatry Philippe Pinel used the word demence to designate one of the five classes of mental derangement. Demence was subsequently translated into the English noun dementia in 1806, and was popularized by Rush in 1812 in his classic Medical inquiries and observations upon the diseases of the mind.
However, by applying the term dementia to idiots, Pinel failed to differentiate differntiate between dementia and mental subnormality. (he used the term dementia in relation to the progressive mental changes seen in some idiots). This was accomplished by Pinels student Esquirol in his 1838 textbook Mental maladies-A treatise on insanity. Esquirol summed up the difference between the demented and the mentally handicapped in the following epigram: The dement is a man deprived of the possessions he once enjoyed, he is a rich man who has become poor. But the defective has been penniless and wretched all his life.
(Mahendra, 10). Furthermore, Esquirol he was also instrumental in the popularization of the term senile dementia. Remarkably, his description of senile dementia is very similar to our present day definition. Interestingly, in distinguished between three varieties of dementia: acute, chronic and senile. Although the terms acute and chronic dementia have since been discarded, his description of senile dementia is remarkably similar to our present day definition. Nonetheless, because disorders such as Schizophrenia have not yet been clearly defined it was difficult to differntiate senile dementia from other insanitys which might be present in the elderly. In 1845 Griesinger proposed that senile dementia was due to a disease of the cerebral arteries, a faulty view whichthat persisted until Alzheimers time. Much of todays basic knowledge about dementia was accumulated throughout the second half of the nineteenth century, and the first decade of the twentieth century. me.
1872 saw Huntington present a paper called On chorea, in which he discussed a typical case of what is now known as Huntingtons disease. Twenty years later in 1892 two significant events occurred. First Pick in a paper called On the relation between aphasia and senile brain atrophy described the case of August H. a 71 year old patient with senile dementia. Although the case is not typical of our present day conception of the disease Pick was given credit for discovering a new disease. The other more significant event in 1892 was Blocq and Marienscos description of scattered silver staining plaques in the cortex of senile patients. These plaques were subsequently named senile plaques (SP) by Simchowitz in 1911. The year 1894 saw Alzheimers first majorbig contribution , a differentiation between senile and vascular (arteriosclerotic) dementia.
Alzheimer described the specific changes observed in arteriosclerotic atrophy of the brain, which resembletally close to what we might call vascular dementia. In 1898 another milestone occurred when Binswanger introduced the term presenile dementia. Thus by the twentieth 20th century significant changes were taking place in our understanding of dementia. The nineteenth 19th century view that there was only one mental disease--insanity-and that dementia was its terminal stage was dispelled by Kraepeeplin in the 6th edition of his textbook Psychiatrie,psychiatrie, published in 1899 (Pitt, 4). Kraepelin separated dementia praecox (a concept he proposed in 1898 in relation to Schizophrenia) from the other dementias (paralytica and organic), and )Senile dementia was included under yet another category calledof involution psychosis (Pitt, 4).
Twentieth Century In 1907 Alzheimer published his landmark case A unique illness involving the cerebral cortex in which he described a fifty-five year old demented woman. The case was very unusual for two reasons: its clinical course, and the discovery of a striking microscopic lesion in the womans brain (Beach, 1987). The clinical course was unusual because of the young age of the patient and the rapidity of degeneration (the patient died within four and a half years of symptom onset). At autopsy neuropathological findings were even more unusual. One quarter to one third of cerebral cortical neurons had disappeared, and many of the remaining neurons contained thick, coiled masses of fibers within their cytoplasm (Beach, 1987). These stained intensely with the Bielschwsky silver method, more so than ordinary neurofibrilsAlzheAlzheimer speculated that a chemical change had occurred in the neurofibrils. Furthermore, noticing that sometimes the tangles were found to occur freely in the brain substance, he suggested that they eventually caused the death of the cells that bore them, leaving the tangle as a marker of the dead cell.
Thus Alzheimer had described for the first time neurofibrillary tangles (NFT), which togther with SP, areone considered to be theof the neuropathologocal halmarks signs of AD (See Appendix 1 for Alzheimers original drawing of NFT). Alzheimer concluded that he discovered a unique entity separate from senile dementia as it was known at that time. However, it was not until 1910 when Kraepelin discussed the condition in the 8th edition of his textbook Ppsychiatrie that ADd gained official recognition. Subsequently in 1911 Simchowitz described another neuropathological hallmark of AD granulovacuolar degeneration, and in 1914 Divry described the amyloid changes. It is apparent than, that the foundations of the dementia syndrome as we know it today were firmly in place, then, 80 years ago.
It was known that dementia usually occurred in older age but sometimes earlier; its principal causes-syphilis, arteriosclerosis, Alzheimers disease-could be identified and distinguished from each other; it was due to brain disease. The second decade of the twentieth century witnessed However, the end of the golden period in dementia research (this only lasted until the 1960s when a renaissance occurred). soon came to an end. URen cites two reasons as the principal causes (Pitt, 6). First the rise of Freuds Ppsychodynamic theory caused American psychiatry to swerve in the direction of psychological explanations.
for mental illness and toward psychotherapy. Secondly Kraepelins brilliant descriptions and solid classifications seemed to leave little room for therapeutic efforts or optimism. Notwithstanding, several key contributions have been made in the Ddark Aages of dementia research. In 1920 Creutzfeldt, and in 1921 Jakob, described cases of dementia with pyramidal and extrapyramidal signs. Although it is now thought that only Jakobs case was typical of the disease the Creutzfeldt-Jakob disease (CJD) wais given to the world.
The year 1936 saw an important change with regards to the diagnosis of AD. Before 1936 it was common practice to provide a diagnosis based on both clinical and pathological characteristics. However, when it became clear that many non-demented people had some senile plaques and neurofibrillary tangles, Jervis and Soltz advised that only clinical criteria would suffice for a diagnosis of AD (Mahendra, 14). In 1948 Jervis published his landmark paper called Early senile dementia in Mongoloid idiocy. Jervis described three individuals with Downs syndrome (DS), aged 37, 42 and 47 years, each of whom had shown a profound emotional and intellectual deterioration in the last few years of life.
At autopsy, all were found to have SPsenile plaques and two also displayed NFT neurofibrillary tangles (Beach, 39). This was the first demonstration of NFTtangles in DS and the first full clinical and pathological copathological correlation supporting an Alzheimer- like syndrome in DS (Beach, 39). Research in dementia began to revive in the early sixties. New causes of the dementia syndrome have been recognized, including, depression, which in the form of psuedodementia may mimic dementia (Kiloh, 1961), progressive supranuclear palsy (Steele et al, 1964) and normal pressure hydrocephalus (Adams et al, 1965), (cited in Pitt, 6). Prior to the As late as 1960s the standard British text on clinical psychiatry could still speak of ddementia was still viewed as a chronic, irreversible and chronic, irreversible and untreatable condition (Mahendra, 14). Accordingly, in the 1960s, several writers in England and urope Germany called for a revision of the concept and emphasized that irreversibility should not be viewed as an essential feature of dementia. Another important change that took place in the 1960s concerned epidemiology.
Prior to the sixties arteriosclerosis was thought to be the predominant cause of dementia, whereasile AD was thought to be rare (Pitt, 12). However, aArteriosclerosis was decisively challengedknocked out of the running as the prime cause of dementia by several reports between 1960 and 1970 (i.e.,Tomlinson, Blessed, and Roth, 1968 and 1970). These reports which demonstrated that arteriosclerosis was greatly overestimated as a cause of f dementia, and that the majority of patients dying with dementia in fact showed the characteristic plaques and tangles of AD. Furthermore, Katzman, in 1976 his often cited editorial of 1976, argued that because of similarity inof the clinical picture and the identical nature of the histopatholgy, distinctions between AD and senile dementia were arbitrary and no longer useful (Pitt, 12). Thus when it was understood that AD and senile dementia arewere the similarame disease with a different age onset, it was clear that AD is a common illness.
not uncommon. In the mid-1970s two important contributions were made. First, Butler in his 1975 book Why survive? Being old in America criticized the widespread notion that senility was a normal part of aging. Butler argued that, senility, when it occurs, was a result of brain disease or depression and was potentially treatable. The extension of this view was that senility was abnormal, land that its usual causes were diseases, not just aging (Pitt, 1987).
Second,ly three different labs (Bowen et al, 1976; Davies & Maloney, 1976; and Perry et al, 1977) reported low levels of choline acetyltransferase, the marker enzyme for acetylcholine (ACh), in the brains of patients who died from AD. ACh deficiency has since been the target of most therapeutic efforts in AD (see treatment). Throughout the 1980s and 1990s two trends have emerged. First, with regards to diagnosis, criteria haves been made stricter. Classification systems like the Diagnostic and Statistical Manual have evolved towards a more precise and comprehensive definition of dementia. Moreover, neuoroimaging techniques are becoming more and more standard, allowing in some cases for a more accurate diagnosis.
Secondly, the past fifteen years have witnessed a substantial growth in genetically based research. For instance one of the genes involved in AD, the amyloid precursor protein (APP), has been localized to a specific segment of chromosome 21 (see risk factors). The search for an Alzheimer gene on chromosome 21 has led to the discovery of a gene for the amyloid precursor protein. This protein in turn has been implicated in producing excessive amounts of Beta/A4 protein fragments which are deposited in the senile plaques. There is some evidence to suggest that the Beta/A4 may be toxic and lead to cognitive deficits.
Epidemiology Dementia is known as the quiet epidemic, but it affects a significant proportion of our population. In 1989 the Canadian consensus conference on the assessment of dementia reported that Canada had about 250,000 cases of dementia (which at the time comprised about 1% of the population), with 25,000 new cases occurring annually It is estimated that Canada currently has about 250,000 cases of dementia, with 25,000 new cases occurring each year (Clarfield, 1989). Jorm et al. (1988) project that until the year 2025 Canada will experience a growth in the prevalence of dementia, more rapid than the rise if the number of elderly aged over 65. Jorm et al.
(1988) project that until the year 2025 Canada will experience a growth in the prevalence of dementia, more rapid than the rise in the number of elderly over 65. The majority of dementia cases are attributable to AD, vascular dementias, or a combination of these (Table 1). In the past there were hopes that up to 40% of dementias had reversible causes. However, recent reports (Clarfield, 1988; Barry and Moskowitz, 1988) suggest that the true incidence of reversible dementias is at the most 11% and is probably far lower, with drugs, metabolic causes and depression accounting for about two thirds of the cases (Clarfield, 1989). Both the prevalence and the risk of developing dementia increase exponentially with age.
According to a model proposed by Jorm et al. (1987) there is a doubling of the prevalence rate every 5.1 years. Overall, there are no significant gender differences in prevalence and incidence rates for dementia as a whole. However, for AD, there is an increased prevalnce in females. Jorm et al.
(1987) estimate a female to male AD prevalence ratio of 1.6. Ethnically there seem to be important differences in both prevalence and subtype of dementia. Prevalence wise, Heyman et al. (1991) found that out of a random sample of 4116 16% of African Americans had dementia compared to only 3.1% of Caucasians. The same study also found that mixed and multi-infract dementias (MID) were more likely to occur in African Americans (26% of dementias in African Americans compared to 14% in Caucasians). Moreover, in both Europe and North America most studies point to AD as the most common dementing illness; whereas in Asia (especially Japan) MID predominates (Morris, 1994). The observed high rate of stroke in Japan is consistent with a high MID rate. Possibly the higher level of stress in Japan leads to more strokes and therefore a higher incidence of MID.
Table 1. Etiology of Progressive Dementia and Approximate Incidence senile dementia of the Alzheimer type 50% Multi-infract dementia 10-15% Mixed SDAT and MID 10-15% Alcoholic-nutritional dementia 5-10% Normal pressure hydrocephalus 5% Miscellaneous: Huntingtons disease, neoplasms, chronic subdural hematomas, Parkinsons disease, Cruetzfeldt-Jakob disease, AIDS, unknown cause 5-20% Life Expectancy and Mortality Estimates The following summary is based on Terrys (1988) review of the Wang (1978) and Barclay et al. (1985) studies. The Wang study examined senile dementia (mean age of onset 71.3 years) and presenile dementia (mean age of onset 53.8 years) survival rates during the 1960s. Senile dementia patients survived on the average 6.0 years, close to half of the expected survival rate (11.1 years) of similarly aged non demented people. Presenile demented patients survived slightly longer an average of 6.9 years, against an expected survival of 22.3 years.
The Barclay et al. Studies examined survival rates in AD and MID patients in the 1980s. The mean survival rates for AD and multi-infarct dementia were 8.1 and 6.7 years respectively. Interestingly, the survival rate of demented women on the whole is significantly higher than that of men. Terry (1988) suggests that the lower survival rate of demented men is due to a higher incidence of MID in men.
Risk Factors Age A variety of risk factors are associated with dementia. As mentioned earlier age is a very big risk factor.Age is the biggest risk factor for developing dementia. According to a model proposed by Jorm et al. (1987) a doubling of the prevalence rate occurs every 5.1 years. For the elderly population aged 65 and above the prevalence of dementia is estimated at about 10%. Whereas in the very elderly it can reach up to 40% (Clarfield, 1989).
Genetics Genetic factors are important in some dementing diseasesseem to play an important role in AD. In HD an autosomal dominant gene on chromosome 4 is directly responsible for the disease. The genetic evidence in AD is less conclusive. Overall, there is an increased occurrence of dementia in family members of AD patients (i.e., Larsson et al. 1963). However, it is not clear if AD is heritable.
On the one hand there are studies (i.e., Breitner et al. , 1988) which have reported a cumulative risk of AD among relatives of patients approaching 50%, thus implying an autosomal dominant mode of transmission (Morris, 1994).and a primary genetic etiology. But, on the other hand, genetically transmitted diseases should be concordant in monozygotic twins,; this does not appear to be the case in AD. For instance both Creasey et al. (1989) and Kumar et al. (1991) have reported three pairs of monozygotic twins who were discordant. Whereas Nee et al.
(1987) only found a 41% concordance rate for AD in 17 monozygotic twins. Farrer et al. (1990) suggest that AD appears as an autosomal dominant in families in which the average age of onset among kindreds is under 58. Supporting evidence for this comes from studies which have linked EOAD with DS (Lezak, 1993). Individuals who are afflicted with Down syndrome and who survive to age 40 almost invariably develop Alzheimer like dementia. During the intermediate and terminal stages of DS the individual suffers from recent memory loss, apraxia, temporal disorientation, and mutism, all of which are also common in AD (Morris, 1994). Thus it is not surprising that four studies have found an increased risk for AD with late maternal age (Morris, 1994). The increased risk of AD to patients born to mothers over 40 is consistent with Down syndrome risk curve (Rocca et al. , 1991).
Both EOAD and DS have been localized to chromosome 21. However, chromosome 21 does not appear to be a very good genetic marker for EOAD (Green book, 104). Recent studies have shown that a defect in chromosome 14 is more likely to be associated with EOAD, but the specific gene(s) have not yet been isolated (Green book, 104). Evidence for genetic predisposition to LOAD has only emerged over the last two years. It is now known that a gene which codes for a lipoprotein called ApolipoproteinE (APOE) in chromosome 19 is involved (Green book, 101). APOE is linked to the type 4 allele (e4).
It has now been proven that an increase risk for dementia is dependent on a strong chemical binding between the main ingredient of SP, the Beta amyloid protein, and the APOE-e4 (Green book, 102). Table 2 summarizes the genetic findings that have been made thus far in EOAD and in LOAD. Table 2. Alzheimers Disease Genetics Chromosome 21 Chromosome 14 Chromosome 19 Onset EOAD EOAD LOAD Risk factor for developing AD Low Higher Highest Specific gene(s) APP Not yet isolated Not yet identified Marker APOE-e4 Note: Reproduced from Berger & Finkel, 1995, Treating Alzheimers and other dementias , New York: Springer publishing Other Risk Factors Corsellis and Brierly (1959) [as cited by Graves & Kukull, 1994] have shown that dementia similar to that seen in AD may occur following a single head injury. In addition, dementia puglistica, (the so called punch-drunk syndrome) develops in some boxers.
Lower education has also been associated with dementia. Animal studies demonstrate a (i.e., Greenough et al. , 1981) demonstrate a positive relation between environmental stimulation and dendritic growth. It is also known that dendritic growth in humans continues throughout life. Possibly lower education is related to a lack of mental exercise, which Thus mental exercise could delay the onset of significant cognitive decline (Graves & Kukull, 1994). Aluminum (Al) has been implicated as a possible neurotoxin, but the evidence is inconclusive (Carson & Butcher, 1992)).
Proponents of the Al neurotoxin hypothesis argue that Al has been shown to accumulate in neurons with neurofibrillary degeneration, and that aluminosilicates accumulate in senile plaques. Critics argue that the abnormal accumulation of Al is an effect, not a cause, of brain degeneration. Another controversial risk factor is depression. Four studies have reported a statistically significant association between a history of depression and AD (Graves & Kukull, 1994). The controversy revolves around the idea that depression is possibly an early manifestation of AD.
There is some research suggesting that individuals with a weakened immune system may be more susceptible to develop AD. Heyman et al. (1984) [as cited by Graves & Kukull, 1994] have found an increased risk of AD associated with thyroid disease in women. However, their findings have not been replicated. Interestingly, there is some evidence to suggest that smoking can have a protective effect from AD. For instance, Duijn and Hofman (1991) [as cited by Graves & Kukull, 1994] have found a negative correlation between smoking and AD in a study involving 198 individuals. Neuropathology For each dementing disease a specific neuropathological pattern is observed. However, due to the limited scope of this essay the discussion will be limited to the most important dementing disease, AD.
Gross Features Several changes are observed at the gross neuropathological level in AD (Mirra & Gearing, 1994). Cortical atrophy is generally observed in the frontal, temporal, and parietal cortex. Sectioning of the brain reveals variable enlargement of the lateral and third ventricles. Disproportionate enlargement of the temporal horn of the lateral ventricle is commonly encountered, with concomitant atrophy of the entorhinal cortex, amygdala, and hippocampus. Microscopic Features At the microscopic level the two most distinguishing neuropathological features a ...
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