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Patients With Alzheimers Disease Health And Social Care Essay

Brain deterioration is a gradual process that in the later part of life causes many cognitive deficits. Consequently, mental disorders like dementia develop in this process. Although most dementia cases occur in age 60 years and above, Dementia of the Alzheimer type in some cases develop in an earlier age range which is 40 to 50 years old. The gradual progression of Alzheimer’s disease causes developing mental impairment which then results to a major change in lifestyle. Since the age range 40 to 50 years old is the period wherein an individual is usually at the peak of his career, Alzheimer’s disease troubles more than just the brain lobes but also the social life of the patient.

Patients with Alzheimer’s disease show symptoms which starts basically with lid forgetfulness and progresses up to the inability to gain new information. Alzheimer’s disease involves six stages. Moreover, each stage causes personality changes in the patient. The progression is usually gradual during the first and last stages while rapid in the mid-term of the progress. The progression ends when the patient turns into a vegetative state and acquires certain disease due to weakened defensive system. Furthermore, this results to death.

With the advancing technology, researchers have found ways to know the manifestation of the disease. Various studies involving the neuropathology of the brain with a developing Alzheimer’s disease have been made. As a result, researchers have found ways to manage the disease. However, a cure to completely distinguish Alzheimer’s disease is still lost in time.

BACKGROUND STUDY OF ALZHEIMER’S DISEASE

History

In an article about Alzheimer’s disease in the website creationwiki.org, it is revealed that Alzheimer’s disease was named after Alois Alzheimer, a German physician who first diagnosed and examined the disease along with Franz Nissl. He graduated with a medical degree in Werzberg in 1987. He was known to be focusing in medical fields such as psychosis, epilepsy, birth control, forensic psychiatry and the dementia of degenerative and vascular origins. After his graduation, Alzheimer met Franz Nissl who is a well known neurologist in the mental asylum where Alois had been studying women diagnosed with serious mental issues. Since he had his first year of work in that mental asylum focused on the field of psychiatry, he grew a passion for neuropathology. Alois Alzheimer and Franz Nissl focused on neuropathology and the normal and pathological anatomy of the cerebral cortex. In the year 1895, Franz Nissl became the world’s top leading German psychiatrist. With this, he was invited in 1895 by Emil Kraepelin to the University of Heidelberg. A few years after his acceptance to the offer, he was able to run a clinic for psychiatry. At this time, Alois Alzheimer was focusing his research on the material of his patients. And in 1902, Emil Kraepelin recognized Alois’ works and invited him to Heidelberg just like Nissl. He then started to become famous and was excelling in the expertise on the field of psychiatry. He did his research in Heidelberg for almost a year and went to psychiatric university in Munich along with Emil Kraepelin. He was then introduced to a fifty-one year old woman named Auguste Deter who became Alois’ main focus of research which then resulted to the discovery of Alzheimer’s disease.

In addition and agreement to that of the article in creation.org, an article about the founder of Alzheimer’s disease in the website www.uic.edu states that Alois Alzheimer was a German professor of Psychology in Breslau. With Franz Nissl, he established the pathologic anatomy of mental illness. In 1904, he published his researches on cerebro arteriosclerosis while in 1911, he published his research on Huntington’s disease. His monumental work on Alzheimer’s disease appeared in 1907.

Richard Halgin and Susan Whitbourne also revealed that Alzheimer’s disease was first reported in the 1907 by a German psychiatrist and neuropathologist, Alois Alzheimer. The document case was of a 51-year old woman complaining of poor memory and disorientation to time and place. Eventually, the woman showed signs of depression and hallucination. She also showed cognitive symptoms of dementia like loss of language and lack of recognition of familiar objects. She was almost unable to move or perform voluntary movements. After the death of the woman, Alzheimer was able to know in her autopsy that most of the tissue in the cerebral cortex had degenerated. Alzheimer also found out that individual neurons had degenerated and formed abnormal clumps of neural tissue.

Butcher and Carson added in Halgins statements that DAT takes its name from Alois Alzheimer. Alois Alzheimer is a German neuropsychiatirst who first described the disease in 1860.

According to an article about Alzheimer’s disease in creationwiki.org, the disease was first diagnosed by Alois Alzheimer on Nov. 4, 1906 to a woman named Auguste Deter. Auguste Deter was a 51-year old woman from Frankfurt, Germany. Alois Alzheimer observed her in the Frankfurt Asylum for a few years before she died. In 1997, Professor Konrad Maurer stumbled upon the original folder with Alois Alzheimer’s notes, picture of Auguste, her brain tissue analysis, a post-mortem report and Auguste’s handwritten words and sentences.

Moreover, an article in the website www.best-alzheimers-products.com has thrown light about this subject by bringing out that in November 1901, Auguste was brought to the City Hospital for Mental Ill and Epileptics in Franfurt, Germany by his husband Karl Deter. Karl says that her behavior has disturbed him a lot in his work. He added that Auguste usually wakes up at night and screams for hours. As time passes, the gradual progression of Auguste Deter’s worsened condition is observed. She shows signs of cognitive decline and hallucinations. Eventually, it is observed that Auguste lost almost all cognitive capabilities. She then died on April 8, 1906 at the age of 55 years old. Her brain was sent to Alois Alzheimer in Munich. The articles also informs us that

The patient file for A. Deter survives today. In it, a note written by the doctor on November 26, 1901 includes this paragraph:

She sits on the bed with a helpless expression. What is your name? Auguste. Your Husband? Ah, my husband. She looks as if she didn’t understand the question. Are you married? To Auguste. Mrs D? Yes,yes, Auguste D. How long have you been here? She seems to be trying to remember. Three weeks. What is this? I show her a pencil. A pen. A purse, key, diary and cigar are identified correctly. At lunch she eats cauliflower and pork. Asked what she is eating she answers spinach. When she was chewing meat and asked what she was doing, she answered potatoes and horseradish. When objects are shown to her, she does not remember after a short time which objects have been shown. In between she always speaks about twins. When she is asked to write, she holds the book in such a way that one has the impression that she has a loss in the right visual field. Asked to write Auguste D., she tries to write Mrs and forgets the rest. It is necessary to repeat every word. Amnestic writing disorder. In the evening spontaneous speech is full of paraphrasic derailments and perseverations.

Description and Diagnosis

Butcher and Carson stated that biologists tells us that even on our very first second in this world, the organs of our body starts to deteriorate with aging. Yet, science has not solved the riddle of aging. With this, the brain as the master organs is not exempted from this. As the brain deterioration and degeneration goes on, mental disorders start to occur in old age which are called senile dementias. But there are also mental disorders associated with brain degeneration that occur in an earlier age. These are called presenile dementias. One senile dementia that sometimes occurs well before old age is the Alzheimer’s disease. Moreover, Alzheimer’s disease is a characteristic dementia syndrome having an insidious effect onset and a gradual deteriorating course that leads to death. Its formal psychiatric diagnosis is primary degenerative dementia of the Alzheimer type (DAT). DAT are normally given when cause or causes of dementia is already ruled out by past examinations.

According to Barlow and Durand, Dementia of the Alzheimer’s type is the increasing impairment of memory and other multiple behavioral and cognitive deficits, affecting language, motor functioning, ability to recognize people or things and/or planning. It is the most prevalent dementia.

Allan Ropper and Robert Brown emphasizes that this is the most common and important degenerative disease of the brain, having to an increasing degree an immense societal impact. Some degree of shrinkage in size and weight of the brain, i.e., ”atrophy” is an inevitable accompaniment of advancing age, but that these changes alone are of relatively slight clinical significance and uncertain structural basis e.g., whether the loss of brain weight is due to a simple depletion of neurons. By contrast, severe degrees of diffuse cerebral atrophy that evolve over a few years are invariably associated with dementia, and the underlying pathologic changes in these cases most often prove to be those of Alzheimer’s disease. The rate of brain atrophy specifically of the hippocampus and medial parts of the temporal lobes is accelerated in the early stages of Alzheimer’s disease and longitudinal studies by magnetic resonance imaging (MRI) can identify individuals who will subsequently develop the disease. These observations have significance in relation to future treatment of Alzheimer’s disease at a stage of potential reversibility.

Furthermore, the now outdated practice of giving Alzheimer’s disease and senile dementia the status of separate diseases was attributable to the relatively to the relatively young age of 51 years old of the patient originally studied by Alois Alzheimer in 1907. Such a division is illogical since theses two conditions, except for their age of onset, are clinically and pathologically indistinguishable. There is, in fact, a smooth, exponential, age dependent increase in incidence after 40 years of age. Whether it is useful to classify separately the differing heredofamilial forms of Alzheimer’s disease is an open question, but these occur infrequently enough that they need not to be differentiated from the native disease for the purposes of clinical work.

Carson and Butcher further informs that the clinical picture of DAT on an individual depends on the nature and extent of brain degeneration, the premorbid personality of an individual, the particular stressors that have been or are in operation and the degree of environmental support.

James Butcher and Robert Carson also reveals that Magnetive Resonance Imaging (MRI) may provide supportive evidence by showing ventricles or widened folds(sulci) of the cerebral cortex indicates brain atrophy.

Consequently in our modern time, the continuing consequences of Alzheimer’s disease have already been alarming. Surviving to at least the age of 65 have been common on patients. This means that after the first decade of the twenty-first century, the first members of the post-World War II baby boom generation will be entering the age range of maximum risk. If this problem is left unsolved, it will consequently result to social and economic problems.

Furthermore, Carson and Butcher emphasizes that the Alzheimer’s disease occur only in old age but for some, DAT is a presenile dementia that begins in 40 to 50 years old. In thses cases, the progress of the disease and its associated dementia is typically rapid. For further emphasis on the age range of Alzheimer’s disease, an article about Alzheimer’s on the website kidshealth.org says “Alzheimer’s disease does not affect kids.”

In addition, Halgin and Whitbourne explained that the progression of dementia of the Alzheimer type on patients usually covers a 5-10 year period. The progression ends when the patient dies caused by complicating disease such as pneumonia. In some cases wherein psychotic symptoms like hallucinations and delusions are present, in early phase of the disorder, the progression of the disorder might have an early cognitive decline.

Carson and Butcher affirms that patients on early onset have rapid disease progress thus in some cases, the patient moves quickly into a state of incoherence verging on delirium. This mental clouding is frequently accompanied by agitation and combativeness which is also an event or stage on Alzheimer patients who survive long enough.

Richard Halgin and Susan Whitbourne explains that subtypes of Alzheimer’s disease are identified by the prominent feature of the medical diagnosis. Some subtypes have prominent features such as delirium, delusions, depression and uncomplicated, which none of the other characteristics apply. Doctors specify one of these subtypes on their diagnose of an Alzheimer’s disease patient.

Moreover, Allan Ropper and Robert Brown discuss that some clinicians attempt to subdivide the Alzheimer dementia syndrome into subtypes. Amnestic defect without lexical-semantic abnormalities represents more than 50 percent of cases. Coworkers observed more prevalent and severe language disorder and more rapid progression in early-onset familial cases. Others point to a disproportionately severe defect in praxic functions and a greater tendency to abnormal EEG findings in such cases. Whether such distinctions represent fundamental differences in the disease process is questionable.

Statistics and Societal Observations

Barlow and Durand disclose that researches suggest that Alzheimer’s disease may be more prevalent among women. In statistics, women show higher survival rate. Since women live longer than men, they are more likely to experience Alzheimer’s disease. A tentative explanation shows the involvement of estrogen. Women lose estrogen as they grow older, so perhaps is protective against Alzheimer’s. A study –the Women’s Health Initiative Memory Study- researched on the hormone use among women and its effect on Alzheimer’s. In its initial findings, the study resulted that women over 65 using a type of combined estrogen plus progestrin known as Prempro and observed a risk of Alzheimer’s.

Moreover, although Alzheimer disease has been described at every period of adult life, the majority of patients are in their sixties or older; a relatively small number have been in their late fifties or younger. It is one of the most frequent mental illnesses, making up some 20 percent of all patients of all patients in psychiatric hospitals and a far larger proportion in nursing homes. In the United States, in 17 series comprising 15,000 persons over the age 60 years old, the mean incidence of moderate to severe dementia was calculated to be 4.8 percent as presented in the study of Wang. Ropper and Brown took note of the research of Schoenberg et. al that in Rochester, Minnesota, the incidence per rate for dementia in general is 187 cases per 100,000 population per year, and for Alzheimer disease, 123 cases per 100,000 annually. These staggering statistics may be viewed from another perspective. The incidence rate of clinically diagnosed Alzheimer’s disease is similar throughout the world, and it increases comparably with age, approximately 3 new cases yearly per 100,000 persons below age 60 and 125 new cases per 100,000 of those over 60. The prevalence of the disease per 100,000 population is near 300 in the group aged 60 to 60; it is 3200 in the 70 to 79 group and 10,800 in those over age 80. In the year 2000, there were an estimated 2 million persons with Alzheimer’s disease in the United States. Prevalence rates, which depend also on overall mortality, are three times higher in women, although does appear that the incidence of new cases is only slightly disproportionate in women. The survival of patients with Alzheimer’s disease is reduced to half the expected rate, mainly because of respiratory and cardiovascular causes and inanition but also for other reasons that are not entirely clear.

Stages of the progression of Alzheimer’s disease

Barlow and Durand explains that cognitive deterioration of the Alzheimer’s disease is slow during the early and last stages. The progress becomes more rapid during the middle stages. The average survival time is 8 years as estimated. A form of the disease which occurs during the 40’s and 50’s is referred to as presenile dementia.

Furthermore, Richard Halgin and Susan Whitbourne state that the first stage of Alzheimer’s Disease involves forgetfulness. The individual forget the names of the people the person previously knows and the places where he has placed things. There will be concerns of mild forgetfulness of familiar objects although no objective deficits in work and social situation. The second stage of Alzheimer’s disease is early confusional. The individual in this stage experiences cognitive deficits such as getting lost when going to familiar places, noticing of forgetfulness of names and words by colleagues and family and having poor reading comprehension and inability to concentrate. Personality changes in the patients include denial of memory problems but anxiety accompanies symptoms of forgetfulness and confusion. The third stage of Alzheimer’s disease is late confusional. The patient in this stage suffere decreased knowledge of current events and ability to travel or handle finances. The patient starts to forget one’s personal history. Persosnality changes include very obvious use of denial regarding memory problems. Flattening of affect and withdrawal from challenging situations are visible on the patient’s attitude. The fourth stage of Alzheimer’s disease is early dementia. Early dementia involves certain cognitive deficits on recalling some important features of current life such as address or telephone number and names of grandchildren and personal facts such as the name of one’s high school. There are also disorientations with regard to time or date. The patient might not need assistance for toileting or eating but the patient can possible experience difficulty on choosing proper clothing. The fifth stage of Alzheimer’s disease is middle dementia. In this stage, the patient suffers cognitive deficits such as forgetting the name of spouse or loved ones, becoming largely unaware of all recent events and experiences and surrounding or the season of year yet can distinguish familiar from unfamiliar people in the environment. The patient becomes totally dependent on spouse or caregiver for survival and fails to follow through on intentions due to forgetfulness of these intentions. Many personality and emotional changes occur including becoming delusional, obsessive and anxious. The last stage of Alzheimer’s disease is late dementia. The individual experiences cognitive deficits such as loss of all verbal abilities, incontinent of urine and inability of the use basic psychomotor skills including ability to work. Personality changes involve complete deterioration of personality and social skills. The individual is almost totally unresponsive to all but simplest form of communication.

Consequently, Richard Halgin and Susan Whitbourne relates that Alzheimer’s disease progresses in stages marked by the deterioration of cognitive functioning and changes in personal and interpersonal relationships. The behavioral symptoms are memory loss, disorientation, decline of judgement, deterioration of social skills and extreme flatness or changeability of affect. Some psychological symptoms are agitation, wandering, hallucinations, delusions, aggressiveness, insomnia, demandingness and inability to adapt.

According to Robert Carcon and James Butcher, the end stages of Alzheimer’s disease involve a depressingly similar pattern of reduction to a vegetative existence and death from some disease due to lessened defensive sources. Prior to this point, a given victim is likely to show one of the several dominant behavioral manifestations like loss of various mental capacities beginning with memory for recent events progressing to disorientation., poor judgement, neglect of personal hygiene and loss of contact with reality to an extent precluding independent functioning as adults. Distinctly psychopathological symptoms such as delusions occur transitory and inconsistent over time if ever it does.

SYMPTOMS

Allan Ropper and Robert Brown explains that the onset of the mental changes caused by Alzheimer’s Disease is usually so insiduos that neither the family nor the patient can date the time of its beginning. Occasionally, however, it is brought to attention by an unusal degree of confusion in relation to a febrile illness, an operation, mild head injury, or taking of medication. Other patients may present with complaints of dizziness, mental fogginess, nondescript headaches, or other vaguely expressed and changeable somatic symptoms.

According to Robert Carson and James Butcher, symptoms often begin with an individual’s gradual disengagement in their active life. There is a narrowing of social and other involvement, a lessening of mental alertness and adaptability and a lowering of tolerance to new ideas. This will then change the individual’s routine. The individual starts to act self-centered and childlike which includes preoccupation with bodily functions of eating, digestion and excretion. With these symptoms developing, symptoms like an impaired memory for recent events, “empty” speech where vague expressions replace meaningful nouns and verbs though grammar and syntax remain intact, messiness, impaired judgement, agitation and periods of confusion starts to occur. Specific symptoms vary from patient to another as well the progression’s rapidity until the terminal stages when the patient is reduced to a vegetative state. In rare instances, the symptoms may reverse and partial function may return though in true DAT this reverse will prove temporary.

An article in regard of Alzheimer’s disease symptoms in the website www.ahaf.org states that common early symptoms of Alzheimer’s disease involves confusion, disorientation, short-term memory, verbal dysfunctions and unexplained mood changes. On average, patients diagnosed with the disease live 8 to 10 years but this disease is observed to last for as long as 20 years.

In addition, Halgin and Whitbourne discusses that symptoms that would lead a physician to hypothesize Alzheimer’s disease rather than other forms of cognitive impairment are: multiple cognitive deficits, one of the following cognitive disturbances: language disturbance, impaired ability to carry out motor activities, failure to recognize objects and disturbance in executive functioning such as planning, organizing or abstracting, gradual onset and continuing cognitive decline, decline from previous level of cognitive functioning and deficits that are not due to other disorders, medical conditions, or substance use exclusively during the course of a delirium.

Furthermore, Allan Ropper and Robert Brown explains that the gradual development of forgetfulness is the major symptoms. Small day-to-day happening are not remembered. Seldom used names are particularly elusive. Little used words from an earlier period of life also tend to be lost. Appointments are forgotten and possessions misplaced. Questions are repeated again and again, the patient having forgotten what was just discussed. It is said that remote memories are preserved and recent ones lost (Ribot’s law of memory), but this is only relatively true; it is difficult to check the accuracy of ancient memories. Albert and associates, who tested the patient’s recognition of dated political events and pictures of prominent people past and present, found that some degree of memory loss extends to all decades of life.

According to Richard Halgin and Susan Whitbourne, another symptom of dementia is Aphasia. Aphasia is the loss of ability to use language. Aphasia is caused by damage to the language and speech area of the brain. This also results to damage and deficits to production and understanding of language. Aphasia has two forms namely Wernicke’s aphasia and Broca’s aphasia. In Wernicke’s aphasia, the individual is able to produce words but has lost the ability to understand them which mean that his verbal communications has no meaning. In contrast, Broca’s aphasia has a disturbance of producing words but the comprehension is still intact.

Moreover, a disturbance in the executive functioning is another symptom. Executive functioning includes cognitive abilities such as abstract thinking, planning, organizing and carrying out behaviors. For example, an individual with the disease when asked ”In what way are a watermerlon and a honeydew alike?” the person will respond, ”I’m not sure, but I guess it is because water and dew are both wet.”

Consequently, Halgin and Whitbourne disclose that the symptoms of Alzheimer’s disease evolve over time. Still, the rapidity of the progression depends on the stage of the disease and the capability or situation of the patient. It is seen that the most rapid deterioration occurs during the middle phase of the disease.

CAUSES

Halgin and Whitbourne affirms that main cause of the disease is the progressive deterioration of the brain which goes with aging. Physical conditions can also cause the Alzheimer’s. Some of which are vascular or circulatory diseases, AIDS, head trauma, psychoactive substances and various neurological disorders.

In addition, Barlow and Durand explains that the cause of dementia of the Alzheimer type include progressive brain damage, evident in neurofibrillary tangles and neuritic plaque, confirmed by autopsy but assessed by simplified mental status examination and involved multiple genes.

In the same way, Ropper and Brown adds that experienced neuropathologists recognize a form of Alzheimer disease, particularly on older patients, in which there are senile plaques but few or no neuronal tangles.

An article entitled “What is Alzheimer’s” on the website www.alz.org explains that abnormal structures namely plaques and tangles are one of the primary cause of damaged nerve cells. It is discussed “Plaques are deposits of a protein fragment called beta-amyloid (BAY-tuh Am-uh-loyd) that build up in the spaces between nerve cells. “ On the other hand, Tangles is emphazed in a definition “Tangles are twisted fiber of another protein called tau(rhymes with “wow”) that build up inside cells.” These two is belived to block network between nerve cells which results to cognitive deficits.

Ropper and Brown raises a problem of the neuropathologist which is to distinguish between the normal aged brain and that of Alzheimer’s disease. It is not usual to find a scattering of senile plaques in individuals who were thought to be mentally normal during life. Henderson and Hubbard studied 27 demented individuals aged 64 to 92 years and 20 age-matched, nondemented controls. In the former, 3 to 38 percent of the hippocampal neurons contained neurofibrillary tangles; in all but two of the controls, the number of hippocampal neurons with tangles fell below 2.5 percent. Hence, the difference between plaques and tangles in the aging brain and in Alzheimer’s disease is largely quantitative.

Furthermore, Halgin and Whitbourne explained that after the autopsy on the brains of the patients with Alzheimer, three characteristic changes are seen in the brain. First, the formation of neurofibrillary tangles in which the cellular material within the cell bodies of neuron becomes replaced by densely packed, twisted protein microfibrils or tiny strands is observed. Second, there is a development of senile plaques throughout the cerebral cortex. Senile plaques are clusters of dead or dying neurons combined together with fragment of protein molecules. Third, granulovascular degeneration in which clumps of granular material accumulate within the neurons occurs. This then results to the abnormal functioning of the brain.

Another study of Robert Carson and James Butcher discusses about the numerous microscopic alteration of the brain’s substance which lead to generalized brain atrophy, which may be visualized by imaging techniques. A more promising observation concerns the neurotransmitter Acetycholine which is essential in the mediation of memory. Evidence suggests that the most affected part of the brain of a patient with DAT is the cluster of cell bodies located in the basal forebrail and involved in the release of Acetycholine. These observations lead to the Acetycholine(Ach) depletion theory of DAT etiology.

An article in the website acetycholine.org explains that Acetycholine is a biochemical that is known as a neurotransmitter. Acetycholine carries synapse between neuron.

Moreover, Robert Carson and James Butcher affirms that the fundamental neuropathology of the Alzheimer brain has three elements: the widespread appearance of senile plaques, small areas of dark-colored matter that are in part of the debris of damaged nerve terminals, the tangling of the normally regular patterning of nuerofibrils within neuronal cell bodies and the abnormal appearance of small holes in neuronal tissues called granulovacuoles which derive from cell degeneration. Observation of these changes requires microscopic examination of the brain tissue specimens which is why unequivocal confirmation of the diagnosis is only accomplished after a patient has died when the brain can be closely examined.

Futhermore, some investigators approached the problem of solving the sources of the primary DAT lesions such as neurofibrillary tangles and senile plaques. Their search resulted to a considerable amount of information. Plaques contains cell debris but their cores consist od a waxy protein substance, designated A4 occurs in other parts of DAT patient’s brain.

An article of Dimitri Agamanolis in the website www.neuropathologyweb.org discusses one cause of Alzheimer’s disease which is neuroinflammation. Evidence leads to the conclusion that inflammatory and immune mechanism are involved in Alzheimer’s disease. “Acute-phase proteins are elevated in serum and deposited in SP’s; microglial cells accumulate around SP’s; and complement components are present in SP’s.” APP is an acute phase protein that when released in the brain tissue causes trauma and other insults. Activated microglial cells settles the effects of neuroinflammation. Activated microglial cells are sources of cytokines and free radical.

Furthermore, Another cause is traumatic head injury. It is observed that boxers, football players and other individuals who have had repeated cerebral disturbances develop dementia and parkinsonism. This observation has been previously called dementia pugilistica which mean the punch drunk syndrome. It is now called the chronic traumatic encephalopathy(CTE). In this case, the brain shows neurofibrillary tangles which are not as typical as neuritic plaques of AD.

In addition, type 2 diabetes is an Alzheimer’s disease contributing factor. With low levels of insulin and insulin resistance in the brain, neurons’energy metabolism is impaired and signaling pathways dependent on insulin and its receptors are affected. Nonenzymatic glycation of proteins is a potents genereator of neurotoxis derivatives that aggaravate oxidative damage. An article of Juliette Janson and Thomas Laedtke in the website diabetesjournal.org further explains this by stating

Alzheimer disease and type 2 diabetes are characterized by increased prevalence with aging, a genetic predisposition and comparable pathological features in the islet and brain(amyloid derived from amyloidb protein in the brain in Alzheimer disease and islet amyloid derived from islet amyloid polypeptide in the pancreas in type 2 diabetes)

With these similarities, it is found that diabetes is a risk factor of Alzheimer’s disease.

Moreover, another contributing factor are free radicals. Free radical causes oxidative stress, mitochondrial DNA mutations and mitochondrial dysfunction. Free radicals compound with the progression of age. “This process is accelerated in AD by the action of AB(a mitochondrial poison and free radical generator) and activated microglia, also a source of free radicals.”

Furthermore, another cause of cognitive deficits in Alzheimer’s disease is called ischemia. Ischemia is a restriction in the blood supply to the the different parts of the body. This is mainly caused by cerebral amyloid angiopathy(CAA), cerebral atherosclerosis and small vessel disease. Most of the patients diagnosed with Alzheimer’s disease are found to have these diseases. It is further explained that

Soluble AB is a potent vasoconstrictor of cerebral vessels. Amyloid deposition on the vascular wall results on loss of smooth muscle and narrowing of the lumen. With the loss of their smooth muscle, cerebral arterioles lose their ability to constrict and dilate in response to regional brain activation. Narrowing of capillaries decreases cerebral perfusion and impairs the blood brain barrier function. Occluded capillaries form the seed of SP’s

This then results to the dysfunction of brain capillary network because of senescence.

According to Esles and Heinemann, one pathophysiological effects of alcohol is the chronic brain syndrome or dementia. This disease disease happens when the brain neurons do not have the capacity for regeneration. This is based on the loss of functioning substances in the brain. Everyone loses brain cell from year to year at a normal rate about 10% of the neurons in every 80 years. But if the losses are accelerated by the excessice intake of alcohol, failure of adaptation happens and the brain cell start to diffuse. This may include and result to fatigue, depression, anxiety and loss of interest.

In addition, Ropper and Brown affirms that several putative epidemiologic risk factor for Alzheimer’s disease such as birth order, mother’s age at birth, family history of Down Syndrome, or head injury seem marginal at best and in some instances may be done to selection bias. Whether low educational attainment is a risk factor for the development of Alzheimer’s disease or conversely, whether cognitively demanding occupations protect against dementia has not been settled.

Robert Carson and Butcher conveys that in some cases, a physical ailment or some other stressful events trigger the disease but usually an individual comes through a demented state almost imperceptibly so it is quite impossible to know the date of onset of the disorder precisely.

EFFECTS OF ALZHEIMER’S DISEASE

Ropper and Brown discussed different effectS of Alzheimer’s on personal behavior and actions. It is emphasized that

Once the memory disorder has become pronounced, other failures in cerebral function become increasingly apparent. The patient’s speech is halting because of failure to recall the needed word. The same difficulty interrupts writing. Vocabulary becomes restricted and expressive language stereotyped and inflexible. Comprehension of spoken word seems at first to be preserved, until it is observed that the patient does not carry out a complicated request; even then it is uncertain whether the request was not understood because of inattention or was forgotten. Almost imperceptible at first, these disturbances of language become more apparent as the disease progresses. The range of vocabulary and the accuracy of spelling are reduced. Finally, after many years of illness, there is a failure to speak in full sentences; the finding of words requires a continuous search; and little that is said or written is fully comprehended. There is a tendency to repeat a question before answering it and later there may be a rather dramatic repetition of every spoken phrase(escholia). The deterioration of verbal skills has by then progressed beyond a groping for names and common nouns to an obvious anomic aphasia. Other elements of receptive and executive aphasia are later added but discrete aphasias of the Broca or Wernicke type are characteristically lacking. In general, there is a paucity of speech and a quantitative reduction in mentation.

Moreover, there will be difficulty in locomotion, a kind of steadiness with shortened steps but with only slight motor weakness and rigidity and a fine tremor can be perceived in patients with advanced motor disability. Ultimately, the patient loses the ability to stand and walk, being forced to lie inert to bed and having to be fed and bathed, and the legs may curl into a fixed posture of paraplegia in flexion.

In addition, skill in arithmetic suffers a similar deterioration. Faults in balancing the checkbook, mistakes in figuring the price of items and in making the correct change including many others will continue to progress to a point where the patient can no longer carry out the simplest calculation. This state is called acalculia or dyscalculia. In some patients, visuospatial orientation becomes defective. The car cannot be parked. The arms do not find the correct sleeves of the jacket or shirt. The corners of the tablecloth cannot be oriented with the corners of the table. The patient turns in the wrong direction on the way home. The route from one place to another cannot be described. There is a loss of the sense of direction. As this state worsens, the simplest of geometric forms and patterns cannot be copied.

Furthermore, Late in the course of the illness, the patient forgets how to use common objects and tools but still retains the necessary motor power and coordination for these activities. The razor is no longer correctly applied to face, The latch of the door cannot be unfastened and eating utensils are used awkwardly. Only the most habitual and virtually automatic actions are preserved. Tests of commanded and demonstrated actions cannot be executed or imitated. Ideational and ideomotor apraxia are the terms applied to the advanced forms of this motor incapacity.

Robert Carson and James Butcher reveals that in a less but not uncommon manifestations of Alzheimer’s disease, the patient develops a decidedly paranoid orientation to the environment, wherein the patient becomes suspicious and often convinced that the people around him/her. This is accompanied by uncooperativeness and verbal abuse. Though themes of malevolent victimization predominate in this form of the disorder, another common form is the jealousy delusion wherein the person consistently accuses his/her spouse who is often of advanced age and physically debilitated is being unfaithful in a sexual manner. Family members can be seen as the door of the foul deeds. Fortunately, physical attacks on the perceptive “evil doers” are rare.

In addition, other patterns in the disease are comparatively infrequent than paranoid orientation. Some patients are confused but amiable usually showing marked memory impairment and a tendency to involve in seemingly pointless activities such as hoarding objects or repetitive performance of tasks like in a ritualized manner. Other patients become severely agitated which sometimes is followed by “hand-wringing” depression. Depressed patients experience extremely morbid preoccupations and delusions that are seen as desert of past sins. In such cases, suicide is a possibility.

MANAGEMENT

Management of behavioral problems

In the article entitled “Alzheimer’s Behavior Problems” by Doug Russell and Suzanne Barston on the website helpguide.org, it explained that cognitive deficits usually causes confusion and disorientation to patients diagnosed with Alzheimer’s disease on middle stages. This results to possible dangers to the patient and the people around them. One of the behavioral the patient might manifest is wandering. In order to reduce incidence of wandering, redirect pacing into productive activities. Let the patient get a lot of exercise or involvement on productive activities. Make the patient comfortable if he or she seems disoriented. If the patient wander in a specific time, try to distract him when that time comes. Make the environment comforting and relaxing to the patient like reducing noise levels so as disorientation will might as well be reduced. Disorientation can also be a product of medications and treatment. Consult doctor if this becomes a problem.

In addition, rummaging around or hiding things is another challenge in taking care of patients with Alzheimer’s disease. To protect your property, make sure to lock room or cabinet containing valuables. If items suddenly disappear, investigate and observe for the usual hiding place of the patient. Do not let the patient get near into wastebaskets and trash cans. Check all wastebaskets in order to make sure that nothing valuable is hidden there before emptying them. To protect the patients from harming themselves, remove or restrict access to dangerous substances. Block unused electrical outlets to prevent the patients to experience electrical accidents.

Moreover, dysfunction of senses usually results to hallucinations. With the patient unable to identify sounds and objects, they can start to think of it as a part of a fantasy. Make the environment simple so as to prevent misinterpretation of the different objects. Avoid letting the patient watch the television to reduce cases of paranoia. When hallucinations occur, do not try to differentiate reality and fantasy. Just might as well discuss the patients’ emotions and try to respond to it. Medications can also help prevent cases of hallucinations or illusions.

Furthermore, Alzheimer’s disease patients als manifests aggressive behaviors. Do not confront the patient regarding the behavior. Patients cannot learn to manage there behaviors. Prevent physical contact with the angry patient. Physical contact usually worsens the violence of the patient. Give the patient some space during those times. Make the patient more comfortable by discussing about a more pleasant topic. Observe patterns of anger and let it be a guide so as prevent usual aggressive episodes. Maintain the calmness in the environment to minimize stress. Do not take care of the angry patient alone. Get some assistance from others.

As the same way as the said behavioral problems, rejection to eating is also evident in Alzheimer’s Disease. In order to manage this behavior, try to encourage them in more physical activities. This will make them feel more hungry. Consider their medications. Discuss with the doctor if the lack of appetite to eat continue. Make the patient feel pleasant at mealtimes. Letting them eat their favorite food on a fancy and colored tableware might improve their appetite. Treat them like a baby. Give them little spoonfuls so that they will not have a hard time to eat. Sing rhymes or tell funny and clean jokes to make them enjoy during mealtime. Pay attention to their capabilities in biting food during, in order to provide right meal for them.

Furthermore, disorders on the nervous system often result to sleeping problems. Patient with Alazheimer’s disease reveal wakelfuness and confusion usually thought out the night. This is called sundowning. In order to manage this problem, make the patient more comfortable at nighttime. Let the patient take up more physical activities during the day. Consider the time for sleeping to keep a routine for becoming ready for bed.

Treatments

An article in www.alzinfo.org reveals that science has not yet found a cure for Alzheimer’s but researches continue to progress. With this, new understandings provided information to know how to prevent or delay the continuous nerve cell damage. Drugs treatment are available to be used in order to manage cognitive dysfunctions of patients with Alzheimer’s. Although these drugs cannot stop the progression of the disease, they can be used to slow it down. Drug therapy is essential in early stages and is involved in the integral aspect of caring for the patient.

The Mayo Clinic points outs a study that found the drug donepezil helped reduce the risk of progression of MCI to Alzheimer’s disease for up to 18 months. Other studies are testing the Alzheimer’s drugs galantamine and rivastigmine.

The Mayo Clinic discusses that researches have found that major risk factors of heart disease and stroke may cause dementia. It is suggested that Having a control over these risk factor can be a treatment to delay Alzheimer’s disease.


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