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Alzheimer's disease - Essay Example

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Hi, my name is Miranda. Tonight, I am going to talk about Alzheimer’s disease. This term will keep coming in tonight’s talk, and we will, henceforth, call this AD. If you would ask me to dedicate this conversation to someone, I would always do it to the caregiver bound by responsibility to a relative who has AD…
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Alzheimers disease
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Alzheimer's Disease Hi, my is Miranda. Tonight, I am going to talk about Alzheimer's disease. This term will keep coming in tonight's talk, and we will, henceforth, call this AD. If you would ask me to dedicate this conversation to someone, I would always do it to the caregiver bound by responsibility to a relative who has AD. Let us have a simple thought experiment. Close your eyes and imagine yourself in a room where a patient of AD stays. He is a relation, you just can't leave him alone. Try spending a morning imagining that you are such a caregiver trying to expunge the smell of soiled bed sheets from you clothes while awaiting a relief visit from a willing relation, who promised she would "sit with him", so you can just have a chance to go shopping. You can't wait to get out of the place in look out for a few sanity-giving hours of normal life. Nobody turns up, and you look to your AD relative, the patient, only to communicate. There is positive eye contact, but all in vain. You realize, he fails to recognize you, and you keep churning this thought yourself. Your ceaseless journey from mouth to anus, bed to wheel chair from twilight to twilight continues ad infinitum, and you get angry, with the patient, the doctor, the relation who told she would come, and at last, on yourself ending with a blame on your fate. What is AD Well, Alzheimer's disease is the worst neuropsychiatic disorder of our time dominating not just Psychogeriatric Wards, but the lives of countless children and spouses who have given up work, friends , and all accustomed ways of normal life to support a relative with AD through the last long years. There lives are tormented; they see themselves to be "chained with corpse." To understand AD, we must know what dementia is. Dementia is a syndrome of global impairment of cognition without any effect on consciousness. Typically, there is increasing forgetfulness and progressively developing incompetence in the normal tasks of daily living like cooking, banking, or shopping, like going to the grocery six times a day, getting supply each time, then wondering why there are heaps grocery in the kitchen. To makes things worse, added to it, there is change in personality, uncharacteristically rude and depressed, with repetitious speech. Alzheimer's disease or dementia is the most common cause of dementia in western countries. The volume of the disease translates into 50% of cases of senile loss of memory occurring over the age of 70 years. Apart from the cost of care giving, the disease also claims heavy emotional toll on family members and caregivers. It was described in 1907 first by Professor Alois Alzheimer in Germany. Going straight from postulations to facts, AD can occur in any decade of adulthood and is considered the most common cause of dementia in the elderly. How can the diagnosis of this deadly disease be made Currently, there are two sets of diagnostic criteria that are used by the medical profession and psychiatrists. They employ either DSM-IV-TR, Diagnostic and Statistical Manual of Mental Disorders, 4th Edition or NINDS-ADRDA, The National Institute of Neurological and Communicative Disorders and Stroke-Alzheimer's Disease and Related Disorder Association criteria for successfully diagnosing this disease. This indicates that there has always been some amount of debate and confusion and as a result some haphazardness in the cookbook of the physicians to be able to reach decisions. Whatever may be the format, lets us try to understand the presentation of the disease, the signs and symptoms of AD that mainly leads to a diagnosis. For the patient, the diagnosis and preferably an early diagnosis matters, not the method to reach it. It frequently presents with a subtle onset of memory loss followed by a slowly progressive dementia over many years. Memory is a function of cerebral cortex gray cells. In this disease, there is gross and diffuse decrease in tissue. The cerebral ventricles, the empty spaces at the core of brain, hence get more space to enlarge. Seen differently, for some reason or other the nerve cells develop inflammatory patches or plaques of amyloid. This involves also the arteries supplying those tissues. They now say that this is genetically predetermined, there are defective genes in chromosomes, 1, 14, 19, and 21, and these express themselves in the form of neurofibrillary tangles that inhibit neurotransmission. To diagnose this disease, the physician must be familiar with the signs and symptoms of AD; at least, he must be able to suspect this. According to Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition or DSM-IV, in the category A1, in the early stages of the disease, the subtle memory loss often is underestimated and termed benign forgetfulness. This may manifest as inability to learn new information or to recall previously learned information. In the category A2, mere presence of any of the following would qualify the patient to have AD. Slowly, the cognitive problems, that is, problems with perception, learning, and reasoning begin to show its true colors, and the result is massive interference with daily activities. There is aphasia or language impairment, especially comprehension and naming of objects. In some, aphasia is apparent even in the early phases of the disease. Since there are word finding difficulties, these patients take recourse to circumlocution, where they express things in indirect ways, rather than using the word "pen", they may use "that which writes on a paper", and this is true even when a formal testing with MMSE or mini mental status examination produces normal results. The language deficit or aphasia may be manifested as impairment in fluency, comprehension, and repetition. There may be apraxia alone or in combination, leading to deficits in performing sequential and habitual motor tasks, such as, dressing, eating, solving simple puzzles, and copying geometric figures despite having an intact motor function on neurological examination. There appears to be no sensory deficit, yet these patients may have gross agnosia, failure to recognize or identify objects. Some fortunate patients have agnosognosia; they are just unaware of these difficulties; some know for they have considerable residual insight yet; they have frustration and anxiety. Change of environment may make them dumbfound, and imagine if this bewilderment happens during a walk or while driving. Most importantly, these patients may have problems in executive functioning, that is, planning, organizing, sequencing, abstracting. These people may fail simple calculations, and ask them time, they won't answer! They may have blindness correlated with involvement of the visual cortex, but they will deny inability to see. These criteria enumerated will lead to decline in social or occupational functioning, which must have been declined from the previous known level; the patient fails to keep track on finances, fails to follow and understand instructions on the job; driving becomes sloppy, shopping awkward, and housekeeping a dangerous event, like may forget to turn off the gas in the kitchen. A bit progressed, these patients are just unable to deliver at work, easily lost, always confused, and this, indeed, calls for supervision. This gradual-onset and continued cognitive decline in absence of other dementic neurological organic disorders, systemic conditions causing dementia, or substance-induced conditions, pins the diagnosis. Surprisingly, these patients retain social graces, routine behaviour, and superficial conversation, and these differentiate them from other psychiatric conditions, and it is necessary to note their absence as well as absence of delirium as per DSM-IV-TR. Advanced and late stages, these patients may remain ambulatory but with loitering with absolute loss of judgment, reasoning, and cognitive abilities. Hallucinations, where people perceive things out of nothing or delusions, where people perceive things aberrantly, may happen in AD. These are superficial but concrete. For example, they can accuse the spouse of infidelity, fail to recognize a high school friend, thinks a visitor a burglar, or get scared at his own image in the mirror. There may be loss of inhibition, they may become belligerent, and these may alter with a very passive mood leading to social withdrawal. They may have problems in sleep-wake cycle, their gait may become shuffling, slowly progressing into rigid, mute, incontinent, bedridden social recluse until they die at the end of this 7- to 8-year roller-coastar for the family members, with infection, malnutrition, or cardiac complications. There is a developed code system for DSM-IV criteria. The pathologic counteraction with drug therapy is unpredictable, yet there are five drugs available for treatment of AD. The first class is cholinesterase inhibitor, donepezil, facilitates memory. The second is memantine, shields the brain from overexposure from glutamate, an excess of which is noted in AD. Other than these, there are galantamine slowing acetylcholine breakdown in the brain and stimulating nicotinic receptors in the brain to protect nerve cells, rivastigmine slowing breakdown of acetylcholine, and tacrine that facilitates neurotransmission. Apart from these, hormone replacement therapy, anti- inflammatory agents, and steroids may be part of a multi-pronged management strategy in this invincible disease. Psychotherapy to keep the patient engaged in family affairs and inspiring the patient to enjoy education and learning may help to some extent. The primary focus of the frustrating treatment is on long-term amelioration of associated behavioral and neurologic problems. As elaborated in the beginning of this talk, the psychological impact of this disease is tremendous. Before considering the impact on the people who take care of these patients, imagine how would you feel when you just cannot remember anything. Note pads and stick pads help, but the family is to be trained to emphasize on the pleasanter side of the life and trained how to deemphasize the unpleasant ones. It takes a toll on the family members who remain scared of accidents, and they remain busy making the household safe. When you don't allow one to drive or don't permit one to take a walk alone, this leads to loss of independence, invokes a change of known environment. This may agitate or confuse the patient further. The family needs to learn communication skills and should know how to provide calm reassurance suppressing their own anxieties and sorrows. This will eventually lead to burnout of the caregiver, and the patients ends up in the nursing home or better still, a daycare facility. AD is a problem, and all related to it, the family, the caregiver, the government agencies, daycare facilities, nursing home staff, and above all the physicians, neurologists, psychiatrists, psychologists have their role to play. Rather than considering it as a trouble, an empathetic, calm composure is expected from all who suffer from this disease, the physician, the caregiver, the family, the psychiatrist, the responsible relations, the theorists, save only the patient himself. The way to conquer something is to overpower it, and threads of knowledge can work as a sword to that end. Reference List Longmore, M., Wilkinson, I, and Torok, E., Oxford Handbook of Clinical Medicine, Oxford University Press, Great Clarendon Street, Oxford, OX2, 6DP, 2004, p. 536. Bird, T. D., Alzheimer's Disease and Other Primary Dementias, Harrison's Principles of Internal Medicine, 14th Ed, The McGraw-Hill Companies inc., 1998, ch. 367, p. 2348 Bird, T. D., Alzheimer's Disease and Other Primary Dementias, Harrison's Principles of Internal Medicine, 14th Ed, The McGraw-Hill Companies Inc., 1998, ch. 367, p. 2348 Mendez, M. F. et al, Pick's Disease versus Alzheimer's Disease: A Comparison of Clinical Characteristics, Neurology 43:289, 1993. Hugh, C. H., Epidemiology of Dementia and Alzheimer's Disease, American Journal of Geriatric Psychiatry, May 1998; 6: 3. Dr. Brown, J., Early Diagnosis of Alzheimer's Disease, Brain, Dec 2000; 123: 2567 - 2568. Bird, T. D., Genetic Factors in Alzheimer's Disease: A review of Recent Advances, Annals of Neurology, 40:829, 1996. Helen Lavretsky and Lang Hai Nguyen, Innovations: Geriatric Psychiatry: Diagnosis and Treatment of Neuropsychiatric Symptoms in Alzheimer's Disease, Psychiatr Serv, May 2006; 57: 617 - 619. DSM-IV-TR Code Revision, http://www.dsmivtr.org/2-3changes.cfm DSM Coordinator, American Psychiatric Association, Division of Research, 1000 Wilson Boulevard, Arlington, Va. 22209-3901 Dr. Royall and R Mahurin, EXIT, QED, and DSM-IV: Very Early Alzheimer's disease J Neuropsychiatry Clin Neurosci, Feb 1994; 6: 62. http://www.dmh.cahwnet.gov/DMHDocs/docs/letters02/02-03_attachment.pdf, DSM-IV Change in Criteria. Read More
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