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Biology 202
2001 Second Web Report
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Parkinson's disease otherwise named the "shaking palsy" in 1817 by James Parkinson affects 50,000 Americans every year. The risk of the disease is higher amongst men giving them twice risk of developing Parkinson's disease compared to women (5). It is not clear why men are more prone to getting the disease, but it may be related to them not having the female hormone estrogen. (5). The general population that is at risk for developing Parkinson's disease are people older than fifty (1,5).The disease is related to a motor system disorder that cause the patient's hands, legs, jaw, face, and arms to tremor. Parkinson's disease may also cause bradykinesia (slowness of movement) as well as a loss of balance, and a difficulty in doing ordinary daily activities such as walking, talking, eating, and writing (1,2,5). How does this disease then affect the I-Function? If we already have all of our learned capabilities stored there then how do we account for such a loss once Parkinson's disease has occurred?
Symptoms associated with the disease such as tremors are very rhythmic and usually ends when the patient is sleeping. The resistance of the body to move causes rigidity in motion and is caused by an imbalance of opposing muscles in the body. Postural instability is a disturbance in the patient's balance and coordination (1). Notice many of these symptoms occur in relation to a certain movement the body makes. This is because it is said our brains control our movements, thus Parkinson's disease must directly affect some aspect of the brain.
By the previous symptoms stated associated with Parkinson's disease it is clear that most would directly link the disease to the brain. Parkinson's disease is caused by a decrease in the nerve cells in the brain that produce the chemical dopamine (1,4). A chemical in the synapse is what breaks down the dopamine levels and once that occurs it continues to try to deplete the little dopamine that is left (4). The importance of the dopamine is so that messages can be relayed steadily between the substantia nigra (movement control center in the brain) and the corpus striatum (part of the brain that helps regulate motor activities) (1,4). In order for normal, balanced movement of the body to occur dopamine and acetylcholine (another chemical messenger) levels must be equal (1,4). This inequality between dopamine and acetylcholine levels is what causes the major symptoms associated with Parkinson's disease. Regardless of Parkinson's disease, are dopamine and acetylcholine levels always the same? If not does that necessarily mean one has Parkinson's disease? Will a ridgidness of movement occur?
The fact that Parkinson's disease has such an enormous affect on the movement of the human body, and we have just learned that the disease is a causation of a chemical imbalance in the brain, attention must be paid to how it is said our brain controls the movement of our bodies. Our brain gathers movement information in the central area of the brain, otherwise known as the striatum. The striatum works in accordance with the substantia nigra and that sends out commands for the body to work in balance (3). These commands leave the brain, travels to the spinal cord, then to the muscles and that helps the body to move (3). Neurotransmitters in the body carry messages throughout the body and dopamine is one of these messengers. When a dopamine message is needed, a dopamine nerve cell produce dopamine packets and the packets move to the end of the nerve cell and deposit the dopamine into the synapse (3). The receiving cell is then stimulated to send the message and this process is repeated. To create smooth coordinated movement of the muscles in the body, a chemical called MAO-B therefore breaks down excess dopamine (3). If this process is interrupted continuos movement will cease and be replaced by rigid, uncontrollable body motion.
A concrete reason for reduction in dopamine producing neurons has yet to be discovered. Therefore the cause of Parkinson's disease is somewhat a mystery. However there have been many suggestions as to why dopamine may degenerate in the brain. It has been suggested that an internal toxin, such as exposure to pesticides and toxins in foods may be the culprit (1,5).
To date there is no cure for Parkinson's disease. Science has yet to provide a method for restoring the lost nerve cells that produce dopamine (4). However, the affects of the disease can be delayed with a drug named deprenyl if given in the early stages of the disorder (2). A better-known drug named L-Dopa is more commonly used and is a chemical found naturally in plants and animals (1). The L-Dopa can help replenish the brains supply of dopamine. L-Dopa does help to reduce symptoms of Parkinson's disease, but it cannot replace cells lost to Parkinson's disease and it cannot stop the progression of the disease (1). There are other drugs that are given to Parkinson sufferers as well, they include: bromocriptine and pergolide, selegiline, anticholinergics, and amantadine (1).
If the I-Function can function without the brain, then why can't a person with "Parkinson's disease" make a smooth rigidless motion? I think about the Christopher Reeves example of him moving his foot although he is "paralyzed." I am not persuaded behavior is necessarily caused by a chemical function of the brain, it is an experience of an experience. Christopher Reeves responded to his foot being pinched by moving it because he learned that behavior. If his eyes had been closed and he had been pinched he would never have moved his foot because not only could he not feel it, but he also could not see what was going on so that he could access his I-Function of learned behaviors associated with someone pinching you. I am not totally convinced that brain equals behavior based on these terms. Therefore I feel that "Parkinson's disease" is term given and it lends too much credit to the function of the brain.
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