This is a research paper on Parkinson's disease. A brief history of the disease, as well as it symptoms will be discussed. Custom research papers on Parkinson's disease are Paper Masters specialty. The thesis statement of Parkinson's disease listed here is just a SAMPLE research paper of what we can provide you in research. Parkinson's disease research papers are always original and we guarantee each research paper, essay, book report or research paper that is sold by Paper Masters will never be resold and is plagiarism-free.
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- The biological effects of Parkinson's disease
- Symptoms of Parkinson's
- Cause and onset of Parkinson's
- Genetics and how they factor in to Parkinson's
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Parkinson’s Disease is the most common serious movement disorder in the world, affecting approximately 1% of the adult population over the age of 60. The disease is the result of progressive loss of neurons in substantia nigra portion of the brain, which produces the general symptoms of tremors. They symptoms can be controlled by a drug regimen with a surgical intervention as an option for patients that no longer respond to drug therapy. There is recent evidence that the disease may be genetic in nature, with duplication of the alpha-synuclein gene linked to the onset of Parkinson’s Disease, its severity and progression. The disorder is named after the physician, James Parkinson, who described its symptoms in an 1817 monograph entitled “An Essay on the Shaking Palsy.”
Parkinson’s Disease describes a syndrome that is characterized by both tremors and rigidity, and is usually asymmetric in that it affects one side of the body more than the other. Symptoms also include bradykinesia, which is slowed ability to start and continue movements and adjust the body’s position. Although motor dysfunction defines the disorder, it also involves other symptoms such as cognitive or psychiatric changes and sleep disturbances. It is general responsive to a dopamine treatment, which may be due to the fact that the disease produces the deterioration of the nigral dopamine neurons during the progression of the disease. The onset of the disease in the majority of cases occurs around the age of 60, although there are cases of younger onset and even cases of juvenile onset. The age of onset often impacts the way in which symptoms develop, with younger victims less likely to experience postural instability.
A resting tremor is often the first symptom of the disorder, and occurs in approximately 70% of the victims. The tremor is generally asymmetric and increases with anxiety, certain types of motor activity and when walking. The resting tremor most appears first in the hands in the majority of cases, although there are some cases in which it first appears in the feet. Bradykinesia is the most disabling symptom of the disease, and has the heaviest impact on fine motor movements such as writing. It also tends to reduce arm movements while walking. Postural instability is manifested by decreasing ability to maintain balance, leading to increase risk of falling and collateral harm caused by the fall. Postural instability is generally an indication of relatively advanced Parkinson’s Disease, with gait becoming slower as the victim has more difficulty maintaining the required level of coordination to walk and stand erect.
Cognitive and psychiatric symptoms also develop in advanced Parkinson’s Disease, with studies indicating that between 40% and 80% of the victims develop dementia in the end stage of the disease. In some individuals, the dementia and the drugs used to treat the disorder can lead to hallucinations and other types of psychotic behaviors. Disturbed sleep is also common in the disorder, with symptoms such as depression, restless leg syndrome impacting the ability of the victim to sleep. In many cases, there is also involvement of the autonomic nervous system that leads to constipation or urinary urgency.
There is no definitive test for diagnosing Parkinson’s Disease, with diagnosis based on the collection of symptoms displayed by the patient that fit the criteria for the disease. In some cases, it is difficult to separate the symptoms of normal aging from those of the disease, with asymmetric tremors used move often to confirm the diagnosis. In addition, other types of diseases result in the individual displaying symptoms similar to Parkinson’s Disease. As a result, the confirmed diagnosis of Parkinson’s disease can be delayed in some cases. In some situations, a diagnosis of Parkinson’s can be confirmed based on the response of the patient to medications. There are also situations in which the symptoms of the disease are induced by the patient taking a certain type of drugs. In these cases the patient is not suffering from Parkinson’s Disease, but rather from a collection of symptoms described as parkinsonism that are similar to the symptoms of the disorder. In most cases, the symptoms abate once the drug is discontinued.
The cause of the symptoms associated with Parkinson’s Disease is the depletion of dopamine produced by the brain due to degeneration of the nerve cells that produce the chemical. Dopamine is a neurotransmitter that stimulates motor neurons, which are the nerve cells that control muscles. By the time that symptoms appear, victims of the disorder have lost 80% or more of their dopamine production capabilities. There is no cure for this condition, with treatment focusing on medications to control symptoms and a surgical intervention in more extreme cases. Levodopa is the primary medication used to treat symptoms and is based on a strategy of dopamine replacement. The drug is converted into dopamine by an enzyme in the brain. Drug regimens can also include the use of dopamine agonists that is used in conjunction with levodopa to mimic the function of dopamine in the brain. There are other drugs that use different strategies to combat the disorder, but all of the treatments have a high potential for substantial side effects. In addition, the drug treatments tend to lose effectiveness over time as the disease progresses.
When medications become ineffective in controlling symptoms or the side effects are severe, surgery may be used to control the symptoms of the disease. Only 10% of the individuals with Parkinson’s Disease are candidates for surgery because of the variety of criteria that are used to screen patients for the somewhat risky procedures. Ablative surgery consists of destroying the brain tissue that is producing the abnormal chemicals that result in symptoms, with various methods such as the use of an electric probe used in the procedure. It is very difficult to estimate the amount of tissue that should be destroyed, increasing the risk that healthy tissue will also be destroyed. Deep brain stimulation is a surgical method that implants an electrode in the brain that temporarily deactivates the activity of the tissue in the area surrounding the electrode. There is a risk that the implant can become infected. A third surgical technique is restorative in nature through transplanting dopamine producing cells into the brain, which are intended to replace the functioning of the cells damaged by the disorder. The source of the cells that are transplanted is important to the success rate, with 90% of fetal transplant cells failing to survive while preliminary studies at this time suggest that pig embryo cells may have a better chance of survival. While the mechanism that produces the symptoms is understood, the reasons behind the degeneration of the dopamine-producing nerve cells in the brain remain somewhat unclear. There appears to be some genetic causes to Parkinson’s Disease, with studies showing that it does tend to run in family lines. Recently, a team of researchers has determined that the duplication of the alpha-synuclein gene may be the causative factor for the disease, with a genetic link to the duplication. The findings of this study suggest that there is a direct relationship between the amount of alpha-synuclein that the body produces and the age of onset of Parkinson’s Disease, its severity and its rate of progression. Other studies have linked point mutation in the gene in the development of familial forms of the disorder. In addition, individuals with triplication of the alpha-synuclein gene have a very early onset of the disorder and uncommonly severe symptoms. While the identification of a genetic link that is causative of the disorder can be of assistance in diagnosis of the disease through more refined diagnostic testing, it does not currently provide assistance with the treatment of the disease. In the future, however, some type of preventive drug regimen could potential reduce the negative impact of the over production of alpha-synuclein on the dopamine producing cells of the brain, with screening for the genetic factor determining whether such an approach is required. At the current time, however, the use of genetic screening and potential methods to inhibit the development of the disease remain speculative.