Parkinson’s Disease Essay

Parkinson’s disease affects millions of people around the world. It can affect up to one million people in the United States and almost six million people around the world (“National Parkinson Foundation”, 2010) It is a disorder that involves the lack of proper movement in individuals who are suffering Parkinson’s disease. It is a neurodegenerative disorder that induces a lack of dopamine in the neurons of the substantia nigra (Pinel, 2008; Dobkin, Rubino, Allen, Friedman, Gara, Mark, & Menza, 2012).

Some fact about Parkinson’s disease is that it is more prevalent in males than in females (Pinel, 2008) and also that the risk of developing the disease is greater with age (Glass, 2012). However, Glass (2012) also suggested that symptoms usually occur after the age of fifty but at least one in twenty people can be diagnosed with Parkinson’s under the age of forty. This section of the research paper will discuss the history of Parkinson’s disease with its founder James Parkinson. Parkinson’s disease was named after its founder, James Parkinson, who was famous or well-known for his Essay on the Shaking Palsy in 1817.

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In this essay, he discussed the cases of paralysis agitans (Pfeiffer, Wszolek, & Ebadi, 2012), which in other, easier words is Parkinson’s disease. James Parkinson’s contributed to society and humanity a lot through not only his essay but also through other means such as politics, mental health, chemistry, and geology (Pfeiffer, Wszolek, & Ebadi, 2012). He was born on April 11th, 1755 to John and Mary Parkinson. His father was an apothecary, which is a person who prepares and sells drugs or medication, and also a surgeon.

Morris (1989) postulated that James helped his father through his career and both wrote many case studies about their work (as cited in Pfeiffer, Wszolek, & Ebadi, 2012). Looking into his family life, James got married to Mary Dale in 1781 and the couple had six children together. One of their sons, John William Keys (1735-1838), became a physician and served as an apprentice to his father. He then worked with his father in medical practice and did so for 12 years after his fathers’ death. John Williams Keys’ son, James Key (1812-1849), in turn, practiced with his father until after his death in 1838.

The Parkinson generations had a lot to offer to medical articles and researches and not only to medical practices (Pfeiffer, Wszolek, & Ebadi, 2012). During his education, he performed rescues for drownings in the London Waterways. For this he obtained the Honorary Silver Medal of the Royal Humane Society in 1777, when he rescued a man who had hung himself (Pfeiffer, Wzsolek, Ebadi, 2012). Not much information is given based on his medical education but his most appreciated work, the Essay on the Shaking Palsy, contributed to medicine greatly.

This essay contributed to the cases of Parkinson’s disease and also provided the symptoms and causes to a whole new disorder, one that was not known or given a name to before. In his book, James describes the Shaking Palsy as: “Involuntary tremulous motion, with lessened muscular power, in parts not in action and even when supported: with a propensity to bend the trunk forward, and to pass form a walking to a running pace: the senses and intellects being uninjured. ” (Parkinson, 1817, p. 1).

Parkinson’s contributions allow future generations of clinicians and researchers to understand the condition of Parkinson’s disease, to develop better forms of treatment, and to possibly find a cure (Pfeiffer, Wszolek, & Ebadi, 2012). The next section will discuss the signs and symptoms of Parkinson’s disease to provide a firm grip on the brain disorder. Signs and Symptoms The findings of James Parkinson lead to a whole new disease that needed help. In his essay, he postulated some of the symptoms and signs that were prevalent to the study and allowed researchers to identify that an individual had Parkinson’s disease.

Researchers have put forward the idea that not all symptoms of Parkinson’s disease are motor related and that there are non-motor symptoms (Pandya, Kubu, & Giroux, 2008). Let us take a look at the motor symptoms first. It is basic to know four main symptoms of Parkinson’s disease that one can identify through observation. They are known as “TRAP”, as identified by the University of Chicago Medical Centre (2012). The “T” in TRAP refers to the tremors that a Parkinson’s patient has. This is the involvement of involuntary trembling of the limbs.

The “R” refers to rigidity, which is the stiffness of the muscles that are needed to have smooth body movements. The third letter, “A” is the akinesia that a patient develops which is basically not starting, or if starting, difficultly to maintain movement when in need to do so. Lastly, “P” refers to the postural instability, that is, difficulty in bending or flexing the limbs or joints, such as making a fist with the hand. This instability also involves a certain walk which is recognizable as the patient is either bending towards one side or unable to walk with their shoulders in a straight position.

The non-motor symptoms are significantly as disturbing as the motor symptoms. These symptoms include sensory, autonomic, cognitive-behavioral, and sleep-related symptoms (Pandya, Kubu, & Giroux, 2008; Chaudhari & Quinn, 2006). The sensory symptoms were those that made one feel ill or sickly. One of these was paresthesia, a symptom which can occur during the time when a female does not have her period. These pains could be described as diffuse and aching and are gradual through numbness, tingling feelings, and changes in temperature (Pandya, Kubu, & Giroux, 2008).

Another symptom of senses was that of small and vision. The sense of small, also known as hyposmia (Chaudhuri & Quinn, 2006), is gradually disrupted and becomes impaired. Olfactory impairment is a sign of early Parkinson’s disease. Vision is also impaired but to what extent Parkinson’s disease is involved, is still a question. Hunt, Sadun, & Bassi (1995) postulated that oculomotor defects such as impairment in visual saccadic movements and muscle rigidity are the difficulties in a Parkinson’s disease patient when it comes to reading (as cited in Pandya, Kubu, & Giroux, 2008).

The next set of symptoms is known as autonomic symptoms. Usually, autonomic symptoms increase with age and intensity of the disease as well as the usage of medication (Pandya, Kubu. & Giroux, 2008). Autonomic symptoms have some symptoms that are put under this category; orthostatic hypotension, cold limbs and sweating, gastrointestinal symptoms, urinary problems, and sexual dysfunction. Orthostatic hypotension is a medical term used to describe low blood pressure which usually results in some people when they stand up (Allcock, Ullyart, Kenny, & Burn, 2004).

Another symptom known as postprandial hypotension is more common in Parkinson’s disease and prevalent during midday meals (Pandya, Kubu, & Giroux, 2008). This symptom causes drastic decline in blood pressure after a meal is taken. The symptom of cold limbs and sweating would be described as it is, that is, an individual’s limbs are cold but their body still manages to sweat (Pandya, Kubu, & Giroux, 2008). Gastrointestinal symptoms include dysphagia, which is the difficulty in swallowing, and sialorrhea, which is excessive salivation. Other symptoms are constipation, risk of aspiration, and drooling.

Constipation affects more than half of patients with Parkinson’s disease (Chaudhuri & Quinn, 2006). Another symptom of the autonomic symptoms is urinary problems. The most common problem would be nocturia, followed by frequency and urgency of needing to urinate. Nocturia is excessive urination at night and most common in men. Lastly, sexual dysfunction, including decreased libido and erectile dysfunction are symptoms of autonomic symptoms (Pandya, Kubu, & Giroux, 2008). Cognitive-behavioral problems can also arise as non-motor symptoms in patients of Parkinson’s disease.

Such problems could be those of depression. It is the most common form of cognitive-behavioral problems and diagnosing it is not an easy task. This is because a lot of its features are like those of Parkinson’s disease, making it hard to identify which feature falls under which category (Pandya, Kubu, & Giroux, 2008). It is also postulated that depression in patients who have Parkinson’s disease are younger and have less motor symptoms than those that are older and would therefore have more motor symptoms (Gallagher & Schrag, 2012). Another example is apathy.

Apathy usually occurs with depression, in which there is a lack of interest- which is in the cognitive domain, lack of motivation- which is in the behavioral domain, and lack of emotion- which is in the affective domain (Pandya, Kubu, & Giroux, 2008). Anxiety disorders are also symptoms of cognitive-behavioral problems and they can occur with depression. These disorders can include generalized anxiety disorder, panic disorder, agoraphobia, and social phobia. In the early stages, up to 62. 9% of Parkinson’s disease patients can symptomize anxiety (Gallagher & Schrag, 012).

Visual hallucinations can be symptoms of cognitive-behavioral problems in which patients, at the beginning, know that they are hallucinating because of their medications but, eventually they lose that insight (Pandya, Kubu, & Giroux, 2008). Dementia, another symptom, is characterized by slow thinking and difficulties in working memory and problem-solving. It is considered a classic Parkinson’s symptom (Pandya, Kubu, & Giroux, 2008). The last set of symptoms for non-motor symptoms of Parkinson’s disease are those of sleep disorders.

The first is excessive daytime sleepiness in which patients tend to feel drowsy and sleepy throughout the day (Pandya, Kubu, & Giroux, 2008). Suddenly falling asleep is frightening, especially when carrying out activities like driving. Another is insomnia, which is the difficulty in falling asleep and can cause various sleep patterns (Gallagher & Schrag, 2012). Restless legs syndrome is a painful feeling in the legs or other parts of the body during rest, especially at night. It is more common in patients with Parkinson’s disease than in the general population (Pandya, Kubu, & Giroux, 2008).

Lastly, vivid dreams are another symptom of sleep disorders in which patients have unpleasant or uncomfortable dreams that make them act out their defense while they are sleeping so it is dangerous for the patient and whoever that is sleeping next to him or her (Gallagher & Schrag, 2012). It is clear that both the non-motor and motor symptoms are of concern when it comes to an individual’s ability to be able to carry out everyday functions and how difficult it can become if these functions become impaired.

The following section of this research paper will discuss the causes and brain mechanisms of Parkinson’s disease and try to provide a biological perspective to the disorder. In this attempt, the anatomy, pathophysiology, and the processes of brain cell death will be discussed along with some of the major causes of Parkinson’s disease. Causes and Brain Mechanisms Parkinson’s disease arises greatly in older adults mainly due to the reason of dopamine not being released by neurons of the substantia nigra.

The dopamine is used as a chemical that provides smooth muscle movement in the body. It works as a messenger to the striatum that is responsible for the movements of the body, balance, and walking (Martinu & Monchi, 2012). However, when the cells of the substantia nigra start to deteriorate, the level of dopamine also decreases which in turn does not send messages to the striatum and causes great difficulty in motor functioning (Shankar, 1998). In general, there is a consideration of two main causes of Parkinson’s disease; one is idiopathic and the other is genetics or inheritance.

Although these two causes will be discussed in detail in a later part of this section, a little information to be given is necessary. The sporadic causes or idiopathic causes are basically causes that do not have proper reasons for Parkinson’s disease to take place (Weintraub, Comella, & Horn, 2008). In addition to this, Weintraub, Comella, & Horn (2008) also postulated that about 90% of cases of Parkinson’s disease are sporadic. The second main cause of Parkinson’s disease is known as genetics or having a genetic origin to the disease.

It is understandable that 10% of patients with Parkinson’s disease are known to have genetics origins. Other than the two main causes, there is a set of secondary causes to Parkinson’s disease. These secondary causes are those of medications and certain conditions (Weintraub, Comella, & Horn, 2008). However, it is understood that these medications can cause Parkinson-like symptoms but not the brain disorder itself (Lieberman & McCall, 2003). The first drugs known to cause Parkinson-like symptoms were used to treat the symptoms of schizophrenia and psychosis (Glass, 2012).

These drugs are known as tranquilizers and include haldol, prolixin, stellazine, and thorazine (Lieberman & McCall, 2003). Drugs that are used to treat symptoms of obsessive-compulsive disorder, psychosis and schizophrenia known as orap, risperidal, and zyprexa also caused symptoms of Parkinson-like symptoms (Lieberman & McCall, 2003). Another drug that was used by young drug users was known as MPTP. It is a synthetic heroin that gives rise to permanent Parkinson-like symptoms. Almost all the motor symptoms become apparent including tremors, rigidity, slowness of movement, postural instability and freezing (Dauer & Przedborski, 2003).

A condition that could elicit Parkinson-like symptoms is known as the Shy-Drager Syndrome. This syndrome consists of chronic degeneration of the autonomic system, much like Parkinson’s disease (Glass, 2012). The autonomic functions that are affected are those of heart rate, breathing, and problems with intestinal, urinary, and sexual functions (Elliot, 2010). Blood vessel disorders could also cause Parkinson’s disease in patients who have had severe strokes or atherosclerosis (Glass, 2012). Atherosclerosis is the hardening of the walls of arteries.

Sometimes, some patients do not have the proper disorder but can show symptoms of it for a period of time until diagnosed appropriately (Glass, 2012). Anatomically, the basal ganglia are a brain mechanism involved in movement. It is located beneath the cerebral cortex and includes five nuclei. These are; the globus pallidus, caudate nucleus, putamen, subthalamic nucleus, and substantia nigra. The globus pallidus is divided into internal and external regions, and the substantia nigra is also divided into two regions: the dorsal (pars compacta) and ventral (pars reticulate) regions.

The caudate nucleus and putamen are together known as striatum (McVey, 2007). The function of the basal ganglia is to prepare the body for voluntary movement. Processing is done for planning, triggering, and organizing the adjustment of the persons’ posture (Martinu & Monchi, 2012). For example, getting up from a chair and to start walking is a voluntary movement. However, when affected with Parkinson’s disease, the basal ganglia can no longer function the way it is supposed to. The basal ganglia contain 80% of the brains dopamine.

Parkinson’s disease is caused by the death of these dopaminergic neurons that project between the striatum and the substantia nigra pars compacta or the dorsal part of the substantia nigra (McVey, 2007). It can be considered that the greater the loss of dopaminergic neurons, the greater the loss of movement in an individual. By the time there is an onset of Parkinson’s symptoms, 60-70% of dopaminergic neurons have already been lost (McVey, 2007). The following figure will show the differences between the normal basal ganglia and the Parkinson’s disease basal ganglia:

Figure courtesy of Dr. Paul Cheney. Coming to pathophysiology, there are two causes of Parkinson’s disease. This part of the section will now go into detail about the idiopathic and genetic causes of Parkinson’s disease. We know that the idiopathic causes are causes with no proper reason. Therefore, the idiopathic causes are not well defined as one does not know to what extent it is a cause of Parkinson’s disease. However, postulations have been made that toxins in the environment could cause Parkinson’s disease (Glass, 2012).

Pesticides, herbicides, and fungicides are implications of risk factors in Parkinson’s disease. These are chemicals from well-water consumptions, rural living, and exposures to agriculture. Some specific toxins have also been discovered from the above broader factors. Paraquat is an example of an herbicide (Pfeiffer, Wszolek, Ebadi, 2012). It is used frequently in developing countries and its inhalation can cause fatal respiratory toxicity in humans and animals. Another toxic chemical, used as an insecticide, is rotenone. It is found in roots and leaves of certain plants.

It easily combines with lipids and is able to pass through the blood-brain barrier (Pfeiffer, Wszolek, Ebadi, 2012). Other toxic chemicals are those of manganese, carbon monoxide, and carbon disulfide (Glass, 2012). Manganese is said to be elevated in the brains of patients with Parkinson’s disease. Manganese has been exposed to millions of people around the world and this exposure increases more and more every day. The excessive intake on manganese from the lungs can build up in the brain (Selinus & Alloway, 2005). Carbon monoxide has its toxic effects in all regions of environment and people.

However, for Parkinson’s to develop due to carbon dioxide exposure, the exposure has to be quite severe for symptoms to start showing. The exposure causes a lack of oxygen to the brain which in turn can bring out symptoms of Parkinson’s disease (Blazer & Steffens, 2009). Lastly, carbon disulfide can also bring about Parkinson-like symptoms. It usually comes in the form of solvents or pesticides and sometimes the toxic effects do not show for years (Selinus & Alloway, 2005). The genetic factors are those that play a role in the rise of Parkinson’s disease. Of this, inheritance may play a specific role.

Between 15 to 25% of people with Parkinson’s disease report that another relative also has Parkinson’s disease (Lieberman & McCall, 2003). Parkinson’s disease, like any other brain disorder, would have either environmental factors or genetic factors that play a role. The genetic factors can only come about through mutated genes or genes that are in some way damaged and can no longer carry out its functions appropriately. One of the first genes associated with Parkinson’s disease lies on chromosome 6 and is named the Parkin gene by the Japanese researchers who discovered it (Lieberman & McCall, 2003).

It is known for its role in digesting proteins. It eats up or destroys old or damaged proteins. When we understand its function we realize that if it stops doing what it does, the process of destruction will slow down and those damaged proteins become toxic to the cells (Pfeiffer, Wszolek, & Ebadi, 2012). In turn, these proteins will oxidize and release toxic free radicals. Free radicals are molecules that come about through the breakdown and oxidation of foods and the natural occurring body chemicals. The molecules that are released are toxic and, therefore need to destroyed (Lieberman & McCall, 2003).

Another gene that is associated with Parkinson’s disease is called alpha-synuclein which is on chromosome 4 and it is responsible for some form of Parkinson’s disease inheritance. It is found in Lewy bodies. These Lewy bodies are small, many-shaded pinkish spheres found in the dying nerve cells of people with Parkinson’s disease (Spillantini, Crowther, Jakes, Hasegawa, & Goedert, 1998). The gene mutation involved in the production of alpha-synuclein will eventually kill the cell, a process known as apoptosis (Pinel, 2008). The last part of this section will discuss brain cell death.

It will consider the processes by which dopaminergic cells degenerate. These processes work hand in hand with environmental factors and also genetic factors if not let alone. Some of these processes are mitochondrial abnormality, oxidative stress, and inflammation (Glass, 2012). Mitochondria are part of the cells that store the energy, which is the oxygen. In other words, the cell would not exist if there are no mitochondria. They absorb about 90% of the oxygen within the body and are responsible for energy production and cell regulation (Schapira & Gegg, 2011).

To make it more intense, if the mitochondria start to degenerate then uptake of oxygen is lost resulting in depletion of oxygen to the brain. The cells will eventually die and increase risk of Parkinson’s disease. Oxidative stress is another process of dopaminergic degeneration. It is considered to be one of the primary initiations or starters of Parkinson’s disease (Zhou, Huang, & Przedborski, 2009). During this process, free radicals are released and try to react with surrounding molecules and end up damaging them (Nikam, Nikam, Ahaley, & Sontakke, 2009).

Once the molecules become damaged, it is hard to maintain peace in the surrounding areas of the brain especially as they can cause depletion of the dopaminergic cells. Thirdly, inflammatory events may also contribute to the increase or instability of Parkinson’s disease (Wullner & Klockgether, 2003). The problem with this is that even though it is considered helpful to an individual as, for example, when a certain part is swelled, or is heated up, one can understand that it is the body’s way of getting treated through nourishment and aid.

However, it is not always that beneficial. This is because the immune system can eventually start to damage its normal tissue thinking that it is a foreign body. This is also known as Necrosis- a process in which damaged neurons break and swell causing damage to other neurons around them (Pinel, 2008). It is then obvious how this will end up and it can cause problems and Parkinson’s disease can come about. Causes of Parkinson’s disease cannot really be pin-pointed but some of its processes or apparent techniques can be found.

However, there is still no proper and solicited reason as to why neurons in the substantia nigra have little dopamine when they are supposed to release a lot as dopamine is a major neurotransmitter (Pinel, 2008). Gold Standard Treatment There are different treatments for Parkinson’s disease. However, not many are considered effective in the long-run for the decline in the progression of the disorder. Some of the treatments that are considered effective would be drug therapy- levodopa, and deep-brain stimulation.

Cognitive-behavioral therapy for patients who develop depression with having Parkinson’s disease is also an effective measure to help patients. Levodopa is used as an effective drug in the treatment of Parkinson’s disease. Patients with early Parkinson’s disease would have a decrease in freezing or initiating movement. Levodopa is a drug that eventually converts into the dopamine needed in the substantia nigra. This drug works effectively with a drug called carbidopa, which helps to prevent the formation of dopamine outside the brain (Evans, 2010).

Levodopa works effectively for reducing symptoms of Parkinson’s disease such as tremors, slowness of movement, improves muscle control and balances walking (Glass, 2012). It helps with the motor symptoms more often. Eventually, long-term use of levodopa will wear off and its dosage will not be enough to reduce motor symptoms (Hammond, Bergman, & Brown, 2007). Patients who have been taking levodopa for a period of five to ten years would need to change medication since its effect will no longer be the same as when he/she first started taking the drug.

Also, a common side effect of taking levodopa for a long period of time is involuntary movement (Pinel, 2008). Deep-Brain Stimulation was then considered more effective once it was apparent that levodopa could not help in the long-term. In this form of treatment, a piece of lead, also known as an electrode is inserted into a small opening in the skull and it then implanted in the brain (“National Parkinson Foundation”, 2010). The place where it is planted is known as the target area which is preferably the thalamus, subthalamic nucleus, and globus pallidus (Hammond, Bergam, & Brown, 2007).

The next component is of the extension, which is an insulated wire that is passed under the skin of the head, neck, and shoulder. Lastly, the neurotransmitter is like the battery pack and is usually implanted under the skin near the collarbone (“National Parkinson Foundation”, 2013). It helps to deliver electrical stimulation to the target areas of the brain that control movement. Lastly, depression, affecting up to fifty percent of patients with Parkinson’s disease, is the most commonly associated non-motor problem (Dobkin et al. , 2012).

The best form of treatment for depression in patients with Parkinson’s disease is Cognitive-Behavioral Therapy. Although this form of treatment works best for short-term encounters, it is still effective. In this, the therapist spends a lot of time teaching the patient to confront negative self-talk and try to decrease it eventually. Other ways are to cease self-attacks and to use cognitive tips to handle strong emotions and to label the internal feelings as something that is not as bad or is at least manageable by the patient (Glass, 2012). Conclusion

All in all, to understand the concept of Parkinson’s disease, one must also understand the various implications involved. These would involve understanding the signs and symptoms, causes and brain mechanisms, and also treatment. However, it is hard to find a treatment that does not affect or disrupt other functions or processes in the body. One day, and hopefully soon, a proper cure comes to invention allowing treatment for people with Parkinson’s disease. In the meantime, coping would help greatly with the disease and probably cause fewer complications during the progression of Parkinson’s disease.


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