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An Exploration of Causes and Treatments
General Psychology 105
19 October 2016
Parkinson’s disease is the second most common neurodegenerative disease. Because of its debilitating effects on the quality of life, being able to treat Parkinson’s is important for many people. As a result, there is a great interest in understanding the mechanisms by which it operates so that new treatments can be devised to counteract its effects. As of yet, there is no known cure for it. The treatments that do exist can only delay its onset and minimize existing symptoms. These treatments generally fall into three categories: therapy using drugs, physical therapy, and deep-brain stimulation through surgery. Each of these treatments has benefits and downsides, and it must be determined for each individual patient what treatment yields the best results in his or her case.
The symptoms of Parkinson’s are many and vary from patient to patient. The most common motor effects are bradykinesia, tremors, difficulty initiating movement, and rigid muscle movements. Bradykinesia, the slowness of normally automatic movements, takes on the form of decreased blinking and swinging of arms, decreased facial expression owing to lack of stimulation of facial muscles, unintelligible speech due to failures in tongue movement, difficulty swallowing normally, vision problems including blurriness and seeing double, a slow gait, and difficulty walking and maintaining a rhythm, even in the early stages of the disease. Tremors most often occur while at rest and usually occur in the fingers or in the lips and chin. The tremors can occur without the person’s conscious knowledge. The difficulty in initiating movements causes “freezing” where the patient cannot initiate a gait, is incapable of taking another step, or stops just short of the destination. This goes along with an inability to recover from disruptions to balance, which can lead to falls. Additionally, muscles are rigid, leading to jerky movements and increased resistance when a limb is stretched. As the disease progresses, many of the symptoms worsen, and new symptoms develop. For example, the tremor tends to increase as time goes on, and the difficulty initiating movements worsens with the passage of time. In the advanced stages, patients have difficulty with simple tasks like walking, talking, and getting dressed. Although Parkinson’s is primarily a motor disorder, there are several non-motor symptoms related to cognition, sleep, and pain. Given the impact of these symptoms on everyday life and the loss of independence as the disease progresses, it is important for people afflicted with Parkinson’s to find some remedy to allow them to continue to live their lives normally.
The basic explanation for Parkinson’s is low levels of the neurotransmitter dopamine in the basal ganglia region of the brain, which is important for initiating and executing movements. These abnormally low levels are caused by the death of dopamine-producing cells. The model of the basal ganglia proposed in the 1980s is that the lack of dopamine there causes the globus pallidus interna to be overly active, which in turn inhibits the motor thalamus and primary motor cortex. It is this suppression of the motor cortex that causes the characteristic slowness. This helps to explains some of the non-motor symptoms since the dopamine-dependent areas of the brain extend far and control many things other than movement. As the disease progresses, the neurodegeneration spreads to the limbic system, amygdala, and hippocampus. However, low dopamine levels in the basal ganglia cannot entirely account for Parkinson’s disease. Recent research indicated that it is a complex condition influenced by many factors. For example, the dopamine levels do not directly account for muscle rigidity or the tremor. The phenomenon of “freezing” is also not well understood since patients typically do not have similar trouble with other complex patterns of movement. Most patients benefit from having other external cues. Not all of the reasons for Parkinson’s are understood. If more is discovered about the mechanisms by which these symptoms are brought about, there will be opportunities for new treatments.
The most straightforward way to treat the disease is to increase the dopamine levels in the brain. The first medical treatments involved injections of dopamine. However, they were ineffective because dopamine cannot penetrate the blood-brain barrier and thus cannot have any effect on the brain. Instead, L-dopa, a precursor molecule that the body can turn into dopamine, is used. In addition to L-dopa, there are a number of other drugs that have remedial effects on Parkinson’s patients.
Dopamine replacement therapy, which uses various drugs, has been shown to help with the symptoms of bradykinesia, rigidity, and tremors. L-dopa is by far the most powerful, effective, and well-tolerated drug available now. It can be used as a treatment by itself. However, it does have several negative side effects. Prolonged use leads to a decrease in effectiveness as it “wears off.” Additionally, L-dopa treatments can themselves cause motor complications and bradykinesia. In other words, when overused, L-dopa can actually exacerbate the symptoms that it is trying to prevent. Additionally, L-dopa is almost no help in treating non-motor symptoms that are completely unrelated to dopamine. The problem of L-dopa causing bradykinesia has led to the development of alternative drugs to delay the onset of such symptoms as long as possible. There are many other beneficial drugs besides L-dopa, which can either be used by themselves or in conjunction with L-dopa. These other drugs act as agonists for dopamine, either by binding to receptors to stimulate dopamine production without themselves being converted to dopamine or by blocking the breakdown of dopamine. While these drugs do have many good effects, their side effects can also be very severe. Physical side effects include hypersexuality, hypotension, nausea, leg edema, and gastrointestinal problems. Psychological effects include impulse-control disorders, such as kleptomania and pathological gambling, and psychosis (such as delusions and hallucinations). Some side effects are reminiscent of schizophrenia, which makes sense given that schizophrenia is characterized by abnormally high dopamine levels. Different patients respond differently to each drug, meaning that the drug regimen is specific to each patient. There is no doubt that all forms of dopamine replacement therapy reduce the severity of impairment, but studies have shown that L-dopa is still the most effective and that all treatments have the side effects of losing their effectiveness and causing motor complications after a few years.
Another effective therapy is physical therapy and a regular exercise routine. Physical rehabilitation can help with ability to move, posture, and ability to retain balance. Research is still not prevalent on the effectiveness of physical therapy, but the studies that have been done show that without a doubt, it has a positive effect. There are several different variations of physical therapy that can be done. The simplest is physiotherapy consisting of just calisthenics. Other methods are strength training (involving things such as leg curls, leg presses, and chest presses) and aerobic training (involving things such as jogging or treadmill-walking). The studies that have been done so far seem to indicate that simple physiotherapy does not cause a marked improvement but that aerobic training and strength training provide a real benefit on top of an L-dopa or dopaminergic drug regimen. This benefit may even come partly from the regularity and progression of intensity. The authors of a pioneering study comparing the different types of physical therapy showed that patients who underwent aerobic or strength training “showed significant clinical improvements in the motor symptoms of [Parkinson’s Disease]” and that physical exercise did more than basic calisthenics to reduce symptoms of bradykinesia and rigidity, causing increased agility, upper and lower body strength, and balance. Information about long-term effects of physical therapy as a treatment is still uncertain, especially given that trials have only been done for no more than a few months at a time. There are no known ill side effects, but it is true that regression occurs if the exercises are not done for a while. Physical exercise has its effect on the health by stimulating more areas in the cortex, which improves blood flow to the brain. Additionally, intense physical exercise seems to have structural impact on the brain by activating certain growth factors and promoting motor, cognitive, and behavioral functions.
A third option for treatment, other than drugs or physical therapy, is stereotactic surgery, also known as deep brain stimulation. It involves implanting electrodes in a patient’s basal ganglia in order to be able to stimulate the subthalamic nucleus. The stimulations gave relief very similar to the relief from an L-dopa injection. In fact, deep brain stimulation is very effective for controlling motor fluctuations and tremors and can help with all dopamine-responsive symptoms. Not enough research has been done on deep-brain stimulation to determine what its side-effects are.
It should be noted that no treatment does anything to counteract neuron degeneration. This is why there is no cure but only different strategies for managing the symptoms. In addition to the common therapies already discussed, there are many more drugs targeting different types of receptors that are being researched. Genetic influence through gene therapy is also being explored. Another possibility is continues L-dopa infusion, which has been shown to reduce fluctuations in patients between experiencing and not experiencing symptoms. This would reduce the likelihood of the complications and side effects associated with discrete doses of L-dopa.
In conclusion, Parkinson’s disease is a complex disorder without a cure that affects many people. The best treatment varies from patient to patient, but in general the best currently-available treatment is a combination of dopamine replacement therapy drugs with a regular physical therapy regimen. Since there are still undesirable side effects to the drug regimens, it seems prudent to wait to begin the drugs until the quality of life has reached such a point that more drastic measures are necessary.
Carvalho, Alessandro et al. “Comparison of Strength Training, Aerobic Training, and Additional Physical Therapy as Supplementary Treatments for Parkinson’s Disease: Pilot Study.” Clinical Interventions in Aging 10 (2015): 183–191. Print.
Gil, Carmen, and Ana Martínez. Emerging Drugs and Targets for Parkinson's Disease. Cambridge: Royal Society of Chemistry, 2014. Print.
Griggs, Richard A. Psychology: A Concise Introduction. New York: Worth Publishing, 2014. Print.
Zsigmond, Peter et al. "Stereotactic Microdialysis of the Basal Ganglia in Parkinson’s Disease." Journal of Neuroscience Methods 207.1 (2012): 17-22. Print.
2a doubt, it has a positive effect. There are several different variations of physical therapy that can be done. The simplest is physiotherapy consisting of just calisthenics. Other methods are strength training (involving things such as leg curls, leg presses, and chest presses) and aerobic training (involving things such as jogging or treadmill-walking). The studies that have been done so far seem to indicate that simple physiotherapy does not cause a marked improvement but that aerobic training and strength training provide a real benefit on top of an L-dopa or dopaminergic drug regimen. This benefit may even come partly from the regularity and progression of intensity. The authors of a pioneering study comparing the different types of physical therapy showed that patients who underwent aerobic or strength training “showed significant clinical improvements in the motor symptoms of [Parkinson’s Disease]” and that physical exercise did more than basic calisthenics to reduce symptoms of bradykinesia and rigidity, causi