DementiaEssay Preview: DementiaReport this essayDementiaDementia 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 bizarre
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.
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) also known as senile dementia Alzheimers type (SDAT) is the predominant cause of senile dementia. Early onset AD (EOAD) is the most frequent cause of presenile dementia, but HD, 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. AD and Picks disease are the best known examples of cortical dementia; whereas HD, Parkinsons disease (PD), and progressive supranuclear palsy (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. MID is a common example of mixed dementia.
Historical developments in dementiaPre-Modern DevelopmentsThe use of the term dementia dates back to Roman times. The Latin word 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 (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 described 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 (Pitt, 1987).
Nineteenth CenturyIt 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. However, by applying the term dementia to idiots, Pinel failed to differentiate between dementia and mental subnormality. 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 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 1845 Griesinger proposed that senile dementia was due to a disease of the cerebral arteries, a faulty view which 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. 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 earliest post-mortem evidence of Alzheimer’s was the autopsy of A. B., in 1893. Although he had already been diagnosed with Alzheimer. The disease had never been recognized or considered at that time.
A paper written in 1927 by Louis D. de Sousa addressed the following questions:
It is possible that a large number of cases of Alzheimer’s will occur in the developing brains of patients who have the disease. Is it possible that some of that rare disease may be genetically inherited? Can the disease be controlled by vaccines, radiation therapy, or genetic changes such as mutation in genes that are more likely to cause Alzheimer’s disease?
There is currently no consensus on the scientific consensus on what is genetically influenced by our own condition.
A study with large number of brain samples, including the hippocampus, showed that the neuroplasticity of the hippocampus correlated with the degree and frequency of Alzheimer’s, a form of dementia. These samples, together with many other large and diverse samples, suggest that the severity and frequency of Alzheimer’s is a function of our unique condition. There are also very large genetic differences in genes responsible for disease.
Dr. M.N. L. Jaffe wrote a paper in 1979 in which research indicated that the Alzheimer’s disease gene p53, which codes for gene expression in the hippocampal region, influences the way in which many of the brain genes (such as the P53 protein) are expressed during development. Genetic tests indicate that the p53 gene is important in regulating cognitive performance and attention, and that this has a profound effect on cognitive function in children with an early condition. The P53 gene also regulates gene expression in the brainstem. A number of genes involved in the generation of the neuroplasticity of the hippocampus that have not been fully understood are known to participate in this mechanism. If this is true, then the neuroplasticity of the brain stem may not be completely understood. However, this discovery is of a major importance to clinicians and researchers who are attempting to understand such issues. This is especially true in Alzheimer’s disease cases. When Alzheimer’s disease is discovered, these findings will not be completely understood and other important research will continue.
There is currently no consensus on the scientific consensus on what is genetically influenced by our own condition. A study that compared hippocampal brain volumes with non-neuronal samples of children with Alzheimer’s is currently underway in the U.K. This team of neuroscientists compared the brains of six adults with AD. Although the total volume of children with AD compared to those without the disease is comparable, the authors report only two brain samples that may have differed significantly in different ages. The neuroplasticity of the hippocampus differs from that of adults with Alzheimer’s dementia and was measured using in vitro cell growth models. Another study of six children with Alzheimer’s found lower volume per volume of hippocampus in children with non-neuronal AD. This may be the result of the differences between AD and adults who have the form of neurodegenerative diseases which are not very common with dementia. Another longitudinal study of young, relatively healthy groups of study participants, which used a number of different measures including the type of diet and smoking conditions, is coming back in the future. These studies find that, contrary to popular belief , young adults with Parkinson’s disease have lower volume in hippocampal blood when compared with healthy controls in terms of volume
The earliest post-mortem evidence of Alzheimer’s was the autopsy of A. B., in 1893. Although he had already been diagnosed with Alzheimer. The disease had never been recognized or considered at that time.
A paper written in 1927 by Louis D. de Sousa addressed the following questions:
It is possible that a large number of cases of Alzheimer’s will occur in the developing brains of patients who have the disease. Is it possible that some of that rare disease may be genetically inherited? Can the disease be controlled by vaccines, radiation therapy, or genetic changes such as mutation in genes that are more likely to cause Alzheimer’s disease?
There is currently no consensus on the scientific consensus on what is genetically influenced by our own condition.
A study with large number of brain samples, including the hippocampus, showed that the neuroplasticity of the hippocampus correlated with the degree and frequency of Alzheimer’s, a form of dementia. These samples, together with many other large and diverse samples, suggest that the severity and frequency of Alzheimer’s is a function of our unique condition. There are also very large genetic differences in genes responsible for disease.
Dr. M.N. L. Jaffe wrote a paper in 1979 in which research indicated that the Alzheimer’s disease gene p53, which codes for gene expression in the hippocampal region, influences the way in which many of the brain genes (such as the P53 protein) are expressed during development. Genetic tests indicate that the p53 gene is important in regulating cognitive performance and attention, and that this has a profound effect on cognitive function in children with an early condition. The P53 gene also regulates gene expression in the brainstem. A number of genes involved in the generation of the neuroplasticity of the hippocampus that have not been fully understood are known to participate in this mechanism. If this is true, then the neuroplasticity of the brain stem may not be completely understood. However, this discovery is of a major importance to clinicians and researchers who are attempting to understand such issues. This is especially true in Alzheimer’s disease cases. When Alzheimer’s disease is discovered, these findings will not be completely understood and other important research will continue.
There is currently no consensus on the scientific consensus on what is genetically influenced by our own condition. A study that compared hippocampal brain volumes with non-neuronal samples of children with Alzheimer’s is currently underway in the U.K. This team of neuroscientists compared the brains of six adults with AD. Although the total volume of children with AD compared to those without the disease is comparable, the authors report only two brain samples that may have differed significantly in different ages. The neuroplasticity of the hippocampus differs from that of adults with Alzheimer’s dementia and was measured using in vitro cell growth models. Another study of six children with Alzheimer’s found lower volume per volume of hippocampus in children with non-neuronal AD. This may be the result of the differences between AD and adults who have the form of neurodegenerative diseases which are not very common with dementia. Another longitudinal study of young, relatively healthy groups of study participants, which used a number of different measures including the type of diet and smoking conditions, is coming back in the future. These studies find that, contrary to popular belief , young adults with Parkinson’s disease have lower volume in hippocampal blood when compared with healthy controls in terms of volume
The year 1894 saw Alzheimers first major contribution