Thursday, February 09, 2012   

GRE Resources
GRE Overview
GRE Exclusive
News & Events
Letter of Recommendation
GRE Preparation
GRE Courses & Exams
GRE Resources
GRE US Universities
GRE Free Downloads
GRE Miscellaneous



Parkinson's Disease





Instead, it is suspected that Parkinson’s usually results from the combination of a genetic predisposition and an as yet unidentified environmental trigger (www.pdf.org, December page 3 2000). For early treatments of Parkinson’s disease, extracts from the belladonna plant were found to help relax stiffened muscles and to quiet tremors and were used in therapy until after World War II, when a number of similarly acting drugs came into use. Discovery of the brain dopamine deficiency in parkinsonian patients - reported in 1960 by researchers at the University of Vienna - brought hope that restoring the dopamine level might effectively treat the disease. Investigators soon found, however, that giving dopamine by itself was completely useless: the substance did not reach the brain because it could not cross the blood-brain barrier, a protective biochemical mechanism by which the body screens agents passing from the blood into the central nervous system. Scientists then turned to levodopa, the substance that is dopamine’s metabolic precursor. Levodopa did cross the blood-brain barrier and could be quickly metabolized into dopamine. In 1970, levodopa was approved for prescription sale. It was the first major breakthrough, but side effects are severe nausea and vomiting because the drug is broken very rapidly in the body, requiring large doses if the substance is to penetrate the brain. According to the NINCDS Research Program pamphlet, some patients experienced toxic side effects from these dose levels that were so severe that the drug had to be discontinued. Researchers soon learned, however , that they could greatly reduce dose levels - and thus cut down on side effects - by giving levodopa in conjunction with a substance that slows its breakdown in the body. Sinemet, a combination of levodopa and the inhibiting substance carbidopa, has been available since 1975. Treatments must be fine-tuned to suit individual patients depending on their symptoms and stage of disease (Tackacs, Toronto Star). For most Parkinson’s disease patients, the levodopa/carbidopa page 4 cocktail still stands as the single , most effective therapy available. Most patients benefit from it: some moderately and some with striking relief from their symptoms - at least for several years. There are a few other drugs available that are also prescribed. Symmetrel, which was originally an anti-flu medication, is thought to block or reuptake dopamine by neurons, or it increases the release of dopamine by neurons, thereby increasing the supply of dopamine in the synapses. When its benefits seem to lessen, stopping the drug for a short time and then reintroducing it seems to provide help once again, according to some clinicians. Tremors can be controlled by prescribing anticholinergics, which act to decrease the activity of the balancing neurotransmitter, acetylcholine. Older patients may not be able to take these drugs because they tend to cause confusion and hallucination.

 

Selegiline or deprenyl have been shown to delay the need for sinemet when prescribed in the earliest stages of Parkinson’s disease, and they have also been approved for use in later stages to boost the effects of Sinemet. COMT inhibitors such as tolcapone and entacapone, represent a new class of Parkinson’s medications. These drugs must be taken with levodopa so they prolong the duration of symptom relief by blocking the action of an enzyme which can break down levodopa before it reaches the brain. Like the symptoms of Parkinson’s disease itself, the side effects of drugs vary from patient to patient. They may include dry mouth, nausea, dizziness, confusion, hallucinations, drowsiness, insomnia, and other unwelcome symptoms. Some patients experience no side effects from a drug, while others have to discontinue its use because of them. When drugs aren’t working, there’s still surgery. The most common procedures page 5 are palliodotomys, in which the surgeon drills through the skull and destroys selected brain cells, and deep brain stimulation, in which electrodes are implanted in the thalamus and connected to a pacemaker-like device. In a palliodotomy, there is a possibility of stroke, partial loss of vision, speech and swallowing difficulties, and confusion. There aren’t many risks with deep brain stimulation. New, controversial forms of surgery, called brain tissue implants, are still in experimental , however, promising results leave researchers hopeful that this surgery will provide a long-lasting treatment for the disease. Jim Finn, a recipient of the disease, has had Parkinson’s disease for twenty years. Three years ago, at age fifty-one, doctors diagnosed him as “end stage” - they could do nothing more for him. That’s when Finn’s doctor approached him about an experimental new treatment in which surgeons would implant millions of fetal pig cells into the brains of Parkinson’s patients. Without hesitation, Finn agreed to the surgery (Sinha & Zang, pp. 77-81). Finn describes the procedure as going through a drive-thru: “Buy some burgers, get some surgery.” The whole surgery actually takes only two-and-a-half hours. Also, patients can be awake the whole time from the use of local anesthesia. The doctors inject the fetal pig cells through an injection syringe guided by a halo-shaped frame bolted to the head. Originally, surgeons used aborted human fetuses to harvest the cells which are needed, but many considered this unethical. Researchers realized these obstacles early on, and so focused on using fetal pig cells instead. The results have been amazing:

 



Discussion Center

Discuss

Query

Feedback/ Suggestion

Yahoo Groups

Sirfdosti Groups

Contact Us

 

 




Privacy Policy | Terms and Conditions | About Us Copyright © 2012. onestopgre.com. All rights reserved