Parkinson’s Disease Precautions Essay Paper

Parkinson’s disease is a progressive neurologic disorder affecting the brain centers that are responsible for control and regulation of movement. It is characterized by bradykinesia (slowness of movement), tremor, and muscle stiffness or rigidity (Katzung, Mastes, & Trevor, 2012).

Don't use plagiarized sources. Get Your Custom Essay on

Just from $13/Page

Order Essay

The major lesion appears to result in a loss of pigmented neurons, particularly those in the substantia nigra of the brain. The substantia nigra is a collection of midbrain nuclei that project fibers to the corpus striatum. One of the major neurotransmitters in this area of the brain, and in other parts of the central nervous system, is dopamine, which has an important inhibiting function in the central control of movement (Brunton, Chabner, & Knollman, 2011). Although dopamine normally exists in high concentration in certain parts of the brain, in Parkinson’s disease it is depleted in the substania nigra and the corpus striatum. Depletion of dopamine levels in the basal ganglia is associated with bradykinesia, rigidity, and tremors (Brunton, Chabner, & Knollman, 2011).Parkinson’s Disease Precautions Essay Paper

Permalink:

Regional cerebral blood flow is reduced in patients with Parkinson’s disease, and there is a high prevalence of dementia. Biochemical and pathologic data suggest that demented patients with Parkinson’s disease may have coexistent Alzheimer’s disease (Connelly & Fox, 2012).

In the majority of patients, the cause of the disease is unknown. Arteriosclerotic Parkinsonism is seen more frequently in older age groups. It may follow encephalitis, poisoning, or toxicity (manganese, carbon monoxide), or hypoxia, or may be drug induced. The disease most frequently attacks persons in their fifties and sixties and is the second most common neurologic disorder of the elderly (Brunton, Chabner, & Knollman, 2011).

Parkinson’s disease (PD) is a long-term degenerative disorder of the central nervous system that mainly affects the motor system.[1] As the disease worsens, non-motor symptoms become more common.[1][4] The symptoms usually emerge slowly.[1] Early in the disease, the most obvious symptoms are shaking, rigidity, slowness of movement, and difficulty with walking.[1] Thinking and behavioral problems may also occur.[2] Dementia becomes common in the advanced stages of the disease.[2] Depression and anxiety are also common, occurring in more than a third of people with PD.[2] Other symptoms include sensory, sleep, and emotional problems.[1][2] The main motor symptoms are collectively called “parkinsonism”, or a “parkinsonian syndrome”.[4][9]Parkinson’s Disease Precautions Essay Paper

The cause of Parkinson’s disease is unknown, but is believed to involve both genetic and environmental factors.[4] Those with a family member affected are more likely to get the disease themselves.[4] There is also an increased risk in people exposed to certain pesticides and among those who have had prior head injuries, while there is a reduced risk in tobacco smokers and those who drink coffee or tea.[4][10] The motor symptoms of the disease result from the death of cells in the substantia nigra, a region of the midbrain.[1] This results in not enough dopamine in this region of the brain.[1] The cause of this cell death is poorly understood, but it involves the build-up of proteins into Lewy bodies in the neurons.[4] Diagnosis of typical cases is mainly based on symptoms, with tests such as neuroimaging used to rule out other diseases.[1]

There is no cure for Parkinson’s disease.[1] Treatment aims to improve the symptoms.[1][11] Initial treatment is typically with the antiparkinson medication levodopa (L-DOPA), followed by dopamine agonists when levodopa becomes less effective.[2] As the disease progresses and neurons continue to be lost, these medications become less effective while at the same time they produce a complication marked by involuntary writhing movements.[2] Diet and some forms of rehabilitation have shown some effectiveness at improving symptoms.[12][13] Surgery to place microelectrodes for deep brain stimulation has been used to reduce motor symptoms in severe cases where drugs are ineffective.[1] Evidence for treatments for the non-movement-related symptoms of PD, such as sleep disturbances and emotional problems, is less strong.[4]

In 2015, PD affected 6.2 million people and resulted in about 117,400 deaths globally.[7][8] Parkinson’s disease typically occurs in people over the age of 60, of whom about one percent are affected.[1][3] Males are more often affected than females at a ratio of around 3:2.[4] When it is seen in people before the age of 50, it is called early-onset PD.[14] The average life expectancy following diagnosis is between 7 and 15 years.[2][6] The disease is named after the English doctor James Parkinson, who published the first detailed description in An Essay on the Shaking Palsy, in 1817.[15][16] Public awareness campaigns include World Parkinson’s Day (on the birthday of James Parkinson, 11 April) and the use of a red tulip as the symbol of the disease.[17] People with Parkinson’s who have increased the public’s awareness of the condition include actor Michael J. Fox, Olympic cyclist Davis Phinney, professional boxer Muhammad Ali, and actor Alan Parkinson’s Disease Precautions Essay Paper

Parkinson’s disease is a condition where the brain over many years progressively becomes damaged by a loss of nerve cells in part of the brain (as shown in figure 1). The main symptoms of Parkinson’s disease are mainly relational to motor movement; a person with Parkinson’s disease may have involuntary shaking of specific parts of the body known as tremor, muscle stiffness which causes everyday tasks to be very difficult such as getting up from a chair known as rigidity and physical movements to become very slow such as walking known as bradykinesia.

It is thought that Parkinson’s disease affects 1 in 500 and the average age for the symptoms to occur is around 60 with rare cases of 1 in 20 cases where it has developed in people aged under 50. It is thought that there are currently 127,000[1]people in the UK alone with the condition and men are more likely to get Parkinson’s than women. Unfortunately there is currently no cure for the disease.

http://i.dawn.com/2010/11/parkinson-brain5431.jpgFigure 1[2]

Brain activities shown in a healthy brain in compare with someone with Parkinson’s disease brain.

Possible solution

Psychoactive drug

Since motor symptoms of the disease are due to lack of dopamine in the substantia nigra[8] which is the part of the brain which gets damaged progressively over many years; Levodopa is a psychoactive drug (able to cross the blood-brain barrier) can used treatment for Parkinson’s disease as it is converted into dopamine in the dopaminergic neurons of the midbrain where the main source of dopamine is, to normal concentrations. Levodopa is the most widely used treatment for over 30 years.

The symptoms of Parkinson’s disease develop gradually. They often start with a slight tremor in one hand and a feeling of stiffness in the body.Parkinson’s Disease Precautions Essay Paper

Over time, other symptoms develop, and some people will have dementia.

Most of the symptoms result from a fall in dopamine levels in the brain.

One study, based in France, found in 2015 that men are 50 percent more likely to develop Parkinson’s disease than women overall, but the risk for women appears to increase with age.

In most people, symptoms appear at the age of 60 years or over. However in 5–10 percent of cases they appear earlier. When Parkinson’s disease develops before the age of 50 years, this is called “early onset” Parkinson’s disease.

Early signs
Here are some early signs of Parkinson’s disease:

Movement: There may be a tremor in the hands.
Coordination: A reduced sense of coordination and balance can cause people to drop items they are holding. They may be more likely to fall.
Gait: The person’s posture may change, so that they lean forward slightly, as if they were hurrying. They may also develop a shuffling gait.
Facial expression: This can become fixed, due to changes in the nerves that control facial muscles.
Voice: There may be a tremor in the voice, or the person may speak more softly than before.
Handwriting: This may become more cramped and smaller.
Sense of smell: A loss of sense of smell can be an early sign.
Sleep problems: These are a feature of Parkinson’s, and they may be an early sign. Restless legs may contribute to this.
Other common symptoms include:

mood changes, including depression
difficulty chewing and swallowing
problems with urination
constipation
skin problems
sleep problems
REM sleep disorder: Authors of a study published in 2015 describe another neurological condition, REM sleep disorder, as a “powerful predictor” for Parkinson’s disease and some other neurological conditions.

Parkinson’s disease (PD) is a progressive neurodegenerative disorder caused by the loss of dopaminergic neurons in the substantia nigra pars compacta of the midbrain. The impaired production and secretion of dopamine causes a variety of symptoms, including bradykinesia, tremor, rigidity, and other motor and cognitive problems. Although the disease was first described in 1817 (Parkinson, 2002), few treatments exist today. These treatments do not target the cause of the disease and instead aim to increase the levels of dopamine.Parkinson’s Disease Precautions Essay Paper

A major difficulty in understanding PD is the complexity of disease onset. Multiple pathways, including protein aggregation, defects in the ubiquitin-proteasome system, mitochondrial damage, and oxidative and nitrosative stress, can all contribute to the loss of dopaminergic neurons (Dawson and Dawson, 2003). How these pathways are activated and interconnected remains a question of the utmost importance.

The protein α-synuclein (α-syn) appears to play a key role in the pathogenesis of PD (Gitler and Shorter, 2007). α-Syn is the major component of Lewy bodies, the pathological hallmark of the disease, and mutations in the α-syn gene (SNCA) cause PD in rare familial forms of the disease. Additionally, duplication and triplication of wild-type SNCA has also been linked to PD.

Most model organisms of PD have been designed to express α-syn because of its prominent role in the disease. These biological tools, which have now expanded to yeast (Outeiro and Lindquist, 2003), Caenorhabditis elegans (van Ham et al., 2008), Drosophila melanogaster (Feany and Bender, 2000) and mammalian models (Masliah et al., 2000), help to define how pathways interact, establish early markers of the disease, and facilitate the discovery of drugs that may slow or prevent the pathology.

Models in yeast or any other organism cannot perfectly recapitulate the disease as seen in humans. However, models have proven to be useful in the past for uncovering key players in human diseases. Two examples of the success of the yeast α-syn model are the Rab GTPase Ypt1 (Cooper et al., 2006) and a putative manganese transporter, YPK9 (Gitler et al., 2009). These proteins were discovered in genetic screens for suppressors of α-syn toxicity and were validated in a variety of animal and cell culture models of PD (Cooper et al., 2006; Gitler et al., 2009). Indeed, the human homolog of YPK9, PARK9, was shown to be involved in the onset and pathology of PD (Gitler et al., 2009; Ramirez et al., 2006). Clearly, the yeast model system is a powerful tool for elucidating the molecular basis for disease pathways.Parkinson’s Disease Precautions Essay Paper

In a recent issue of DMM, Su et al. utilize a yeast strain expressing toxic levels of α-syn to examine transcriptional differences and to screen for small molecules that reduce toxicity (Su et al., 2009). The authors found that α-syn overexpression affected the transcriptional profile and morphology of yeast cells. Transcriptional characterization of the α-syn-expressing cells showed significant changes in transcription long before cell death had occurred. Genes involved in mitochondrial function and maintenance were downregulated, whereas oxidoreductase genes were upregulated (see fig. 1 in Su et al.). The morphological hallmarks of α-syn overexpression included lipid droplet accumulation, endoplasmic reticulum (ER)-Golgi trafficking defects, misshapen mitochondria, high levels of reactive oxygen species (ROS), and accumulation of cytoplasmic α-syn foci (see fig. 2 in Su et al.). These are significant findings because they connect the yeast model of α-syn aggregation with several key neuronal phenotypes of PD.

A major breakthrough described by this paper arose out of an extensive small molecule screen examining the effect of over 100,000 chemical compounds on α-syn toxicity in yeast. A group of four 1,2, 3,4-tetrahydroquinolinone compounds [denoted (1), (2), (3) and (4)] emerged from the screen as suppressors of α-syn toxicity (see fig. 3A in Su et al.). In α-syn-expressing cells, the bioactive compounds prevented many transcriptional changes caused by α-syn expression. Importantly, the compounds ameliorated the symptoms of α-syn aggregation: ROS levels decreased, α-syn foci vanished, ER-Golgi trafficking resumed, and mitochondrial morphology was restored. The structurally related compounds (5) and (6) did not act as suppressors of α-syn toxicity, but did competitively inhibit the bioactive compounds, suggesting that all of the tetrahydroquinolinones tested bound to the same target(s).Parkinson’s Disease Precautions Essay Paper

Although they were unable to elucidate the exact mechanism of action of the bioactive molecules, the authors were able to rule out a few possibilities. First, the compounds were specific antagonists of α-syn toxicity because they did not affect cell viability in yeast carrying a toxic polyQ construct. This suggests that the compounds were not general modulators of the cellular stress responses caused by protein aggregation. Second, the bioactive molecules did not affect levels of α-syn in vivo, or aggregation of α-syn in vitro, which the authors interpreted as evidence that the compounds did not directly influence the expression of α-syn, or directly interact with α-syn, respectively. Finally, the authors showed that the compounds were not simply acting as free radical scavengers because the antioxidants N-acetylcysteine, riboflavin and melatonin did not alter α-syn toxicity in the yeast model.

To extend their findings and determine whether the α-syn toxicity suppressors from their yeast screen were efficacious in vivo, the authors tested compounds (1–6) in a nematode model of PD. The nematode C. elegans is an attractive model system because the expression of α-syn in its neurons results in an age-dependent loss of dopaminergic neurons, a phenotype that closely resembles that seen in humans (Cao et al., 2005). Compounds (1–4), but not compounds (5–6), were found to suppress α-syn toxicity. For the most bioactive compound, (1), this suppression resulted in a 20% increase in the number of worms with all four dopaminergic neurons. Remarkably, the bioactive compounds were also able to partially reverse the phenotype of worms that were expressing α-syn for two days prior to treatment (see fig. 4 in Su et al.). This observation is particularly exciting because it means that these compounds might hold promise for treating the disease once it is initiated, rather than having to treat before the onset of symptoms.

To determine whether their findings were relevant to mammals, the authors used embryonic rat midbrain cultures transduced with α-syn-A53T, a variant of α-syn linked to early-onset PD. Expression of the A53T mutant induced reproducible cell toxicity. Additionally, surviving neurons displayed aberrant morphology. The compounds (1–3) and (6) were potent suppressors of α-syn toxicity in these rat midbrain cultures, resulting in an increase in the relative number of dopaminergic neurons. Neuron morphology also remained normal. Compounds (4) and (5) did not affect α-syn toxicity (see fig. 4 in Su et al.). Interestingly, compounds (1) and (4), and to a lesser extent (3) and (5), prevented rotenone-induced toxicity (see fig. 6 in Su et al.). Rotenone is a mitochondrial complex I inhibitor that is often used to model PD-like mitochondrial damage in rodents. This finding is significant because it illustrates that the compounds can cure PD symptoms that are not directly caused by α-syn aggregation.Parkinson’s Disease Precautions Essay Paper

The results presented in this article are exciting; however, it is still unclear whether the bioactive molecules are truly effective at reversing aberrant cell phenotypes after the α-syn aggregation has caused cellular toxicity. Although rescue experiments were performed in C. elegans with positive results, it is necessary to perform these studies in other systems to show that the compounds are able to reverse the α-syn phenotype and not simply prevent it. Effective PD drugs need to be administered after the onset of disease, not before. Additionally, the cellular target of the bioactive compounds is unknown, and there is not enough evidence to conclude that the compounds are not interacting with α-syn itself. Understanding how these molecules work could reveal much about the etiology of PD. Affinity chromatography with immobilized bioactive compounds could be used to identify their in vivo targets. Targets might also be identified by using chemical-genetic profiling in yeast (Parsons et al., 2004; Parsons et al., 2006). In this technique, libraries of haploid deletion mutants would be screened with the drugs to identify hypersensitive strains. Comparisons with known chemical-genetic profiles and genetic interaction maps could then be used to elucidate possible target pathways and illuminate the mode of action of these compounds.

The initial causes of PD are not fully understood. Although α-syn can clearly play a role in the development of the disease, multiple pathways are intimately linked: oxidative damage, proteasomal impairment, α-syn aggregation, mitochondria dysfunction and ER-Golgi trafficking defects may all contribute to the death of dopaminergic neurons. Although Su et al. (Su et al., 2009) do not offer insight into all aspects of this complex network of disease pathology, their results are very encouraging and bring us one step closer to the possibility of treating various cellular symptoms of PD with a single drug. In a broader sense, the work of Su et al. implies the existence of a target that is common to multiple pathways implicated in PD. Although currently elusive, this target presents an ideal therapeutic site.

Parkinson’s Disease (PD) is a central nervous system disorder in which the region of the brain that controls movement deteriorates. This neural deterioration results in decreased dopamine levels, the brain chemical that controls coordinated movement.Parkinson’s Disease Precautions Essay Paper

Dopamine plays a major role in a variety of mental and physical functions, including:

Voluntary movement
Cognition
Mood
Memory
General behavior
Parkinson’s now afflicts roughly 1.5 million people in the United States alone, with primary symptoms being body tremors, slow movement, rigid limbs, reduced memory, a shuffling gait and speech impairment. So we have to ask:

1.) What causes it?

2.) How do we prevent it?

Currently there isn’t a known cure, and it’s not fully understood what causes the dip in dopamine; however, we know that aging is the single most important risk factor for PD, with inflammation and stress contributing to cell damage. And we now know enough about the disease to understand the preventative measures that counter the aging and death of the neurons under attack.

Because there is no known cure, it’s critical that we prevent the disease before symptoms arise. Granted, thanks to recent advancements in modern surgical procedures, there are some safe surgeries that can mitigate some of the more severe symptoms associated with PD. The most common one now is deep brain stimulation, in which they implant an electrode into the brain that can stop some of the more severe symptoms of Parkinson’s.

But this article will try to keep it from getting to that point. The less drugs and surgery we can have in our lives, the better.Parkinson’s Disease Precautions Essay Paper

7 Ways to Prevent Parkinson’s Disease
Go Organic (and Local)
Pesticides and herbicides have been heavily implicated in causing Parkinson’s. Researchers have found high levels of pesticides/herbicides in the brains of Parkinson’s sufferers, compared to those with regular dopamine levels. Furthermore, agricultural workers who find themselves exposed to these pesticides have significantly higher rates of PD than the general public.

But while organic is generally a safer bet than conventional, there are still some pesticides and herbicides farmers can legally use on their crops while hanging onto that organic label. This is why knowing the origin of your food is more important than ever before, so get to know your local farmers, join community-supported agricultural programs (CSAs), or start your own garden patch – the best kind of local.

Plus, if you’re concerned about your carbon footprint, keep this in mind: The average foodstuff is shipped 1,500 miles before it finds itself on a supermarket shelf. That’s a lot of fuel to deliver what you can find in your backyard or around the corner.

Eat Fresh, Raw Vegetables
If you needed more reasons to eat your vegetables, this should be the clincher. Studies show that increased amounts of the B vitamin folic acid, found primarily in vegetables, can significantly reduce the risk of Parkinson’s.

The best sources of folic acid are simultaneously some of the healthiest foods on the planet, namely dark green vegetables like broccoli, spinach, collard greens, brussels sprouts, asparagus and okra – all of which can be grown in your backyard! This B vitamin can also be found in avocado, legumes and lentils.

Incorporate Omega-3 Fatty Acids Into Your Diet
Parkinson’s is inflammatory in nature, so researchers have spent much of their time exploring the anti-inflammatory effects of omega-3 fatty acids on the disease. Omega-3 fatty acids are strongly implicated in the prevention of cell degeneration and death, with their benefits going well beyond Parkinson’s prevention.Parkinson’s Disease Precautions Essay Paper

A 2008 study in Canada all but proved the effectiveness of omega-3 fats in preventing Parkinson’s. Researchers in the study gave one group of mice omega-3 supplementation for 10 months and kept one group of mice as a control before injecting them with a chemical that would cause PD.

The results? The control group experienced a steep decline in dopamine levels, while the group that received omega-3 supplementation experienced no decline in dopamine levels and exhibited no signs of Parkinson’s.

Omega-3s have the added benefits of balancing cholesterol levels, boosting immunity, and enhancing cardiovascular health. Your primary sources of this fatty acid are wild-caught fish (especially mackerel, salmon and cod), pastured eggs and walnuts.

Vitamin D3
Vitamin D comes from only two sources:

Sunlight – With the help of cholesterol and vitamins, vitamin D is changed chemically and absorbed into the bloodstream.
Animal Fat – Eating animal fat from healthy animals that are wild or grass-fed is a premier source of vitamin D.
Without enough vitamin D, you can’t absorb the amounts of calcium or phosphorous your body needs to function properly, resulting in a host of negative effects that become more prevalent as we age.

Researchers have found that about 70 percent of early, untreated Parkinson’s patients have low levels of vitamin D – identifying this statistic as a strong correlation would be an understatement.

Other benefits of vitamin D:

Helps boost immunity
Improves bone health and prevents osteoporosis
Necessary for mineral absorption in the body
Protects against dementia
Protects against cancer
Boosts energy and mood
Green Tea
The inherent antioxidant properties of green tea are well known, and the benefits of this tasty drink seem to be boundless:Parkinson’s Disease Precautions Essay Paper

Anti-inflammatory
Nutrient-dense
Reduces risk of cancer
Increases ability to burn fat
Improves brain function
Multiple studies have shown that the certain compounds in green tea have myriad protective benefits on the neural network of the brain. Green tea has also been shown to sustain dopamine levels in ailing brain tissue, reducing the severity of Parkinson’s symptoms for those already diagnosed.

When shopping for green tea, it’s important to choose a higher quality brand, as some of the lower quality brands contain excessive levels of fluoride, which has been shown to have degenerative effects on brain function.

Regular Aerobic Exercise
In addition to physical benefits like increasing lung capacity, bone density and overall longevity, exercise has a distinct impact on brain health. Regular aerobic exercise reduces inflammation in the brain, helping to counter the inflammatory signals leading to the development of Parkinson’s.

A study conducted at the University of Illinois in 2011 clearly showed how modest but regular aerobic exercise can improve our overall cognitive health. Older adults who participated in the study took 40-minute walks three days per week in the course of one year. In that year alone, the participants saw a two-percent increase in the size of their hippocampus, the area of the brain involved in memory and learning. In contrast, without exercise, older adults can expect to see a decrease in the size of their hippocampus by about one or two percent each year.

Given Parkinson’s degenerative effect on cognitive function and memory, the importance of regular exercise cannot be overstated.

CoQ10
CoQ10 is a coenzyme found in the bodies of most animals, including your own. Your cells use it to produce the energy for more cell growth and maintenance, functioning as an antioxidant and protecting those same cells from damage caused by free radicals.Parkinson’s Disease Precautions Essay Paper

Deficiencies in CoQ10 have been shown to contribute to age-related neurodegenerative conditions like Alzheimer’s and Parkinson’s, and patients with PD have been shown to have low levels of this crucial coenzyme in their platelets, plasma and vital regions of the brain. A variety of studies have demonstrated that CoQ10 supplementation can slow the progressive deterioration of Parkinson’s and prevent dopamine loss.

CoQ10 is found in abundance in organ meats like liver, kidney and heart, as well as grass-fed beef and wild-caught fish. Some vegetables, including spinach, broccoli and cauliflower contain CoQ10, but nothing close to the amounts found in organ meats.

CoQ10 must be consumed along with healthy fat to enable absorption of the coenzyme, making the consumption of organ meats – high in healthy fats – a no-brainer. It can also be consumed as a dietary supplement.

Parkinson’s disease is a degenerative neurological disease that affects approximately one million persons in the United States. It primarily impacts the specific part of the brain that controls movement called the substantia nigra. This degeneration creates a shortage of the brain-signaling chemical (neurotransmitter) known as dopamine, causing impaired movement. Symptoms of Parkinson’s disease include trembling (tremor), stooped posture, muscular stiffness (rigidity), short shuffling steps, speaking softly in a rapid tone, poor balance, poor handwriting, and slowness of body movements (bradykinesia). The cause of Parkinson’s disease is not yet known although there may be a genetic link. Some researchers believe it may result from toxins, head trauma or stroke. Presently there is no cure for Parkinson’s disease but available medications control the slow decline in function and manage symptoms quite effectively.
Parkinson’s disease is usually diagnosed in people in the prime of their life. Unfortunately, this also usually means that Parkinson’s strikes during the peak of the individual’s career. Parkinson’s involves the gradual death of cells in the substantia nigra. In the early stages, a very large percentage of the cells die before the deficiency of dopamine becomes severe enough to cause trouble and causes the remaining functional cells to work overtime. Many times, consequences of aging present themselves much like the symptoms of Parkinson’s. There is no specific examination that provides a definitive diagnosis such as a chemical test or a x-ray study. Therefore, the physician’s examination includes tests of sensation, movement, and balance, which probe for signs of damage to the nervous system.Parkinson’s Disease Precautions Essay Paper

Most of us at one time or another have noticed our hands tremble when we are holding a drink, or our teeth chatter when it is very cold out. This is normal. Sometimes though a small tremor is one of the first signs of Parkinson’s disease.
Parkinson’s disease is a chronic, progressive, movement disorder that affects muscle control and balance. These symptoms gradually worsen over time, and generally other secondary symptoms start to occur.
How your brain coordinates movement and what can go wrong
Parkinson’s disease is caused by a gradual deterioration in the function of nerve cells, or neurons, located in a specific area of your brain. Your brain contains millions of neurons, which process and transmit information. It receives information via neurons from all parts of your body, processes it, and then sends out instructions to other parts of your body to produce specific actions. The information travels along neurons as electrical impulses. When a nerve impulse reaches the junction between two neurons, a chemical neurotransmitter (think of it as a bike courier carrying information from one building to the next) is released that stimulates the impulse in the next neuron so that it continues on to its destination.
Image of neutotransmitters traveling across a synaptic junction
Image of neutotransmitters traveling across a synaptic junction
Several different areas of your brain are used to process and transmit the information that controls movement, and a malfunction in any of these can cause a movement disorder. With Parkinson’s, the malfunction occurs within an important movement control centre in the midbrain called the substantia nigra. Normally, the neurons in this region produce a neurotransmitter called dopamine. In Parkinson’s, clumps of protein known as Lewy bodies build up inside the dopamine producing neurons, which steadily degenerate and eventually die. The death of dopamine producing neurons means less dopamine, and without enough dopamine other parts of your brain cannot operate properly. Ultimately, this makes walking, reaching for objects and other basic movements very difficult. Additional loss of dopamine in other regions of your brain and in your intestines, is thought to be at least partly to blame for some of the secondary symptoms of Parkinson’s.
What are the symptoms of Parkinson’s?
The primary symptoms of Parkinson’s are related to movement, and vary from one person to the next. Sometimes at the onset of Parkinson’s, you may not even be aware that you have any symptoms. Gradually though, and usually over a period of years, symptoms do become noticeable, and are often of three distinct types:Parkinson’s Disease Precautions Essay Paper
tremors – these will typically start in one hand on one side of your body, but you may also feel them in your arms, legs, jaw and face.
bradykinesia – this is when your movements become slower, making it very difficult to perform even simple tasks.
rigidity – this is when your muscles are unable to relax, which can affect your posture and make your movements are more jerky. You may even find yourself freezing like a statue in the middle of what you are doing (akinesia).
As the disease progresses, as well as getting slower, Parkinson’s often causes characteristic changes in the way you walk. As a result, you may find you have difficulty starting to walk, are only able to take small shuffling steps, and then have difficulty stopping walking. This is known as Parkinsonian gait. All of the problems with movement are usually accompanied by muscle stiffness that can occur in any part of your body, limit your range of motion, cause you pain, change your posture and disrupt your balance.
There are also many secondary symptoms of Parkinson’s that are not related to movement. Most of these fall into three major categories, autonomic or involuntary symptoms, cognitive and psychiatric symptoms, and sleep disorders; for example, you may lose your sense of smell, find you are sweating a lot, have signs of depression, or have trouble sleeping. However, because every case is unique, it is impossible to predict which of these you might experience. That said, psychiatric symptoms such as nightmares, hallucinations and dementia often become more problematic in the later stages of the disease.
Image showing the symptoms of Parkinson’s Disease
Image showing the symptoms of Parkinson’s Disease
Why do some people get Parkinson’s and not others?
We don’t know what causes the dopamine producing neurons to die in Parkinson’s disease, or why this happens to some people and not others. We do know though that it is very rare when you are young, usually doesn’t start until middle age or later in life, affects men more than women, and seems to run in families. We also know there is a connection between Parkinson’s and head trauma, as well as exposure to some pesticides and solvents. Overall however, none of these risk factors alter the chances you will get Parkinson’s by very much at all.
How common is Parkinson’s?
Overall, around 300 per 100,000 people have Parkinson’s disease. Most people are diagnosed during their 70s; although 15% of cases occur among people who are under 50 years of age. Recent estimates indicate that the number of people living with Parkinson’s steadily increases with age Parkinson’s Disease Precautions Essay Paper
1
start superscript, 1, end superscript Given this, it is clear that the burden of Parkinson’s disease is set to increase in many countries as the population ages.

Figure 2[3]

http://www.epda.eu.com/EasysiteWeb/getresource.axd?AssetID=3455&type=full&servicetype=InlineThe figure shows the process of the administration of levodopa through time scale and the effectiveness of the symptoms being relieved and reduced below the threshold line where the symptoms appear.

Only around 5-10% of levodopa actually crosses the blood-brain barrier, whereas the remainder is metabolised to dopamine elsewhere in the body and cause adverse effects such as nausea, dyskinesias and joint stiffness. However by being paired with Carbidopa or benserizde it prevents the metabolism of levodopa to dopamine before it reaches the dopaminergic neurons, hence reducing the side effects but not completely.

Publication of trial ‘Levodopa and the Progression of Parkinson’s Disease’ by The Parkinson Study Group [4] on a sample size of 361 concluded that carbidopa-levodopa (paired) slows the progression of or has a prolonged effect on the symptoms of the disease. In comparison to a placebo group as a control, Parkinsonism was significantly increased more in the placebo group than with patients administered at different concentrations of carbidopa-levodopa (see figure 3).

Figure 3[4]

Improvement in Parkinsonism is represented by lower scores, and worsening by higher scores. Negative scores on the curves indicate improvement from baseline. The bars indicate the standard error.

Implications

Economic

People who have Parkinson’s disease may be restricted to the confines of their own homes as they may not even have the mobility to get up from a chair without help from another person. Due to the inability of someone being beside people with Parkinson’s all the time to help this causes economic pressure towards the NHS to provide sufficient technological advances to aid what is estimated to be 127,000 people which is a huge mass of money to go into development. In addition to this, the technology itself requires maintenance costing even more money.Parkinson’s Disease Precautions Essay Paper

Social

Developing on the point of being restricted into the confines of their own homes, this raises the risk of losing social interactions of the outside world. Due to the inability to meet with family or friends every so often they want makes the individual feel alienated and lonely, which is one of the causes for depression. They will feel like they have lost their own life and power to do anything due to nothing of their own fault and this is ever more particular in the case that an individual has no more ties.

Ethical

Treatment towards Parkinson’s disease has adverse effects which may be hugely unpleasant for the individual; it is vital that they are supported by care workers, friends and family in order with dealing with Parkinson’s as it what they will have to overcome for years in order to gain what they can of living a normal life. If there isn’t sufficient support then the patient will reject any further treatment as they feel it is too unpleasant to deal with.

Alternatives

Dopamine agonists

Dopamine agonists have seen to have similar effects to levodopa on the brain and are mainly used as target towards delaying motor complications and when used in late Parkinson’s disease they are useful in reducing the off periods (figure 2, when the curve is below the line this is considered as the off periods as the effects of the drug has not been motion).Parkinson’s Disease Precautions Essay Paper

The graph shows comparative results between the effects of dopamine uptake in the brain and medication. The dopamine uptake is relational to the ‘off’ time. The results from the graph show that dopamine agonists (pramipexole and ropinirole) have a much more significant effect against in reducing symptoms than the psychoactive drug levodopa at around 50% dopamine uptake in comparison to only 10%.

http://www.neurology.org/content/62/2/343/F1.large.jpg

Compared with levodopa, dopamine agonists may delay motor complications of medication use but are less effective at controlling symptoms. Dopamine agonists also produce side effects such as drowsiness, insomnia, constipation, nausea and hallucinations which may be felt significant but usually mild. In addition, agonists have been related to impulse control disorders such as compulsive sexual activity, pathological shopping and gambling more so than levodopa. Furthermore, treatment of Parkinson’s disease through the use of dopamine agonists is more expensive than levodopa treatment.Parkinson’s Disease Precautions Essay Paper

Deep Brain Stimulation

DBS (Deep brain stimulation) involves surgical treatment of implanting a brain pacemaker, a medical device that sends electrical impulses to specific parts of the brain. Due to this DBS helps to alleviate the motor fluctuations and tremor symptoms of Parkinson’s disease. However this approach of treatment is generally recommended for people in advanced stages of Parkinson’s disease of which the effects of drug therapy are no longer effective.

DBS is often not the choice of option as neurological surgery is unpredictable in adverse effects which include compulsive gaming, depression, hallucinations and furthermore potential complications of surgery such as bleeding within the brain. Even after the surgery, patients will suffer swelling of the brain, sleepiness, disorientation and eventual removal of sutures [7].

Rehabilitation

There is evidence that mobility problems can improve through rehabilitation however the studies are deemed to be scarce and low quality [6]. Doing regular physical exercise/activities through physiotherapy is beneficial as you gain improved strength, mobility and flexibility and this in turn improves your quality of life by being less constricted to Parkinson’s diseases motor movement symptoms as you gain more control.

Exercises such as these have shown improvements in motor function for people with Parkinson’s disease tend as they tend to have long areas of inactivity. There are even respiratory improvements due to posture and deep diaphragm breathing exercises necessary for physical exercise as this improves vital capacity and chest wall mobility.Parkinson’s Disease Precautions Essay Paper

Parkinson disease (PD), also referred to as Parkinson’s disease and paralysis agitans, is a progressive neurodegenerative disease that is the third most common neurologic disorder of older adults. It is a debilitating disease affecting motor ability and is characterized by four cardinal symptoms: tremor rigidity, bradykinesia or kinesis (slow movement/no movement), and postural instability. Most people have primary, or idiopathic, disease. A few patients have secondary parkinsonian symptoms from conditions such as brain tumors and certain anti-psychotic drugs.

The clinical manifestations of Parkinson’s disease are impaired movement, muscle rigidity, tremor, muscle weakness, and loss of postural reflexes. Early signs include a stiffening of the extremities and a wax-like rigidity in the performance of all movements. The patient has difficulty in initiating, maintaining, and performing motor activities, and experiences some delay in carrying out normal activity (Kofman).

As the disease progresses, the tremor begins, frequently in one hand and arm, then the other, and later in the head, although the tremor may remain unilateral. The tremor is characteristic: it is a slow, turning motion (pronation-supination) of the forearm and the hand, and motion of the thumb against the fingers as if rolling a pill between the fingers. It increases when the patient is concentrating or feels anxious (Connelly & Fox, 2012).

Other characteristics of the disease affect the face, stature, and gait. There is loss of normal arm swing. Eventually, the rigid extremities become weaker. Since there is limited movement in the muscles, the face has so little expression that it is said to be masklike (with infrequency of blinking), a feature that can be recognized at a glance (Connelly & Fox, 2012).

There is a loss of postural reflexes, and the patient stands with head bent forward and walks as if in danger of falling forward. Difficulty in pivoting and loss of balance may lead to frequent falls (Katzung, Mastes, & Trevor, 2012).Parkinson’s Disease Precautions Essay Paper

Frequently, these patients show signs of depression, and it has not been established whether the depression is a reaction to the disorder or related to a biochemical abnormality. Mental manifestations may appear in the form of cognitive, perceptual, and memory deficits. A number of psychiatric manifestations (personality changes, psychosis, dementia, confusion) are particularly common among the elderly (Kofman). Complications from immobility (pneumonia, urinary tract infection) and the consequences of falls and accidents are major causes of death (Kofman).

Early diagnosis of Parkinson’s disease can be difficult, as the patient can rarely pinpoint when symptoms started. Often someone close to the patient notices a change such as stooped posture, stiff arm, a slight limp, or tremor. Handwriting changes may be an early diagnostic clue. The diagnosis of Parkinson’s disease can usually be made with certainty when there is evidence of tremor, rigidity, and bradykinesia (Brunton, Chabner, & Knollman, 2011). The results of the patient’s history and neurological examination are carefully evaluated. Without treatment Parkinson’s disease progresses over ten to fifteen years to a rigid, akinetic state in which patients are incapable of caring for themselves (Brunton, Chabner, & Knollman, 2011). The availability of effective pharmacological treatment has altered the prognosis of Parkinson’s disease; in most cases, functional mobility can be maintained for many years. Life expectancy of adequately treated patients is increased substantially (Brunton, Chabner, & Knollman, 2011). The presence of dysphagia is associated with shorter survival times. Motor impairment of the muscles in the throat impairs swallowing and poses a risk for aspiration pneumonia. Other complications of Parkinson’s disease include sleep disorders, sexual dysfunction, bowel and bladder complications, and sensory problems, such as the loss of smell (Kofman).Parkinson’s Disease Precautions Essay Paper

There is no cure for Parkinson’s disease. Treatment mainly relies on replacing dopamine with focus on controlling symptoms and improving quality of life (Katzung, Mastes, & Trevor, 2012). Because Parkinson’s disease symptoms are due to a deficiency of the brain chemical dopamine, the brain drug treatment help increase dopamine levels in the brain. Levodopa, usually in combination with carbidopa, is the standard drug treatment (Katzung, Mastes, & Trevor, 2012). For patients who do not respond to levodopa, dopamine agonists may be prescribed. Physical therapy is an important part of Parkinson’s disease treatment. Rehabilitation can help improve balance, mobility, speech and functional abilities. No treatment method has been proven to change the course of the disease. For early disease, with little or no impairment, drug therapy may not be necessary (Kofman).

There is no cure for Parkinson’s disease, but medications, physical therapy, and surgical interventions can help control symptoms and improve the quality of life (Connelly & Fox, 2012). The goals of treatment are to relieve disabilities and balance the problems of the disease with the side effects of the medications. A number of issues must be considered in choosing a medication for treatment. These include the effectiveness of the medication, the side effects of the medication, and the loss of effectiveness over time (Brunton, Chabner, & Knollman, 2011).

Levodopa (L-dopa) has been used for years and is the gold standard for treatment. L-dopa increases brain levels of dopamine. It is probably the most effective drug for controlling symptoms and is used in all phases of the disease. The standard preparations, Sinemet and Atamet, combine levodopa with carbidopa, a drug that slows the breakdown of levodopa. Levodopa is better at improving motor problems than dopamine agonists but increases the risk of involuntary movements. Effectiveness tends to decrease after four to five years of use (Brunton, Chabner, & Knollman, 2011).

Dopamine agonists’ drugs mimic dopamine to stimulate the dopamine system in the brain. The drugs included are pramipexole (Mirapex), ropinirole (Requip), bromocriptine (Parlodel), and rotigotine (Neupro) (Katzung, Mastes, & Trevor, 2012).Parkinson’s Disease Precautions Essay Paper

Monoamine oxidase B inhibitors may have some mild benefits in initial therapy; they include selegiline (Eldepryl) and rasagiline (Azilect), and they slow the breakdown of dopamine that occurs naturally in the brain and dopamine produced by levodopa (Katzung, Mastes, & Trevor, 2012).

Entacapone (comtan) is a catechol-o-methyl transferase (COMT) inhibitor that helps to prolong the effects of levodopa by blocking an enzyme that breaks down dopamine (Brunton, Chabner, & Knollman, 2011).

Medications to treat other symptoms associated with Parkinson’s disease include antidepressants. Tricyclic’s, particularly Amitriptyline (Elavil), studies indicate that the use of SSRIs may worsen symptoms. Anti-psychotics include clozapine and quetiapine help with psychotic symptoms seen with Parkinson’s disease (Brunton, Chabner, & Knollman, 2011). The cholinesterase inhibitor drugs donepezil (Aricept) and rivastigmine (Exelon) are used to treat Alzheimer’s disease and are sometimes used for Parkinson’s disease. The benefits are small and may not be noticed. Daytime sleepiness and fatigue may be treated with modafinil (Provigil) a drug used to treat narcolepsy or methylphenidate (Ritalin) may be considered for fatigue. Glycopyrrolate, scopolamine, and injections of botulinum toxin may be used to relieve drooling symptoms (Brunton, Chabner, & Knollman, 2011).

Advanced Parkinson’s disease poses challenges for the patient and caregivers. Eventually, symptoms such as stooped posture, freezing, and speech difficulties may no longer respond to drug therapy. Surgery (deep brain stimulation) may be considered. Patients become increasingly dependent on others for care and require assistance with daily tasks. The goal of treatment for advanced Parkinson’s disease should be on providing safety, comfort, and quality of life (Brunton, Chabner, & Knollman, 2011).Parkinson’s Disease Precautions Essay Paper

The toxic effects of Levodopa with carbidopa are considerable. Dyskinesia, the ability to control muscles, can take many forms, most often uncontrolled flailing of the arms and legs or chorea, rapid and repetitive motions that can affect the limbs, face, tongue, mouth, and neck (Brunton, Chabner, & Knollman, 2011). Hypotension is a common problem during the first few weeks of therapy. Cardiac arrhythmias and gastrointestinal difficulties are common, with the potential of gastric bleeding. Levodopa can cause disturbances in breathing function, but may benefit patients with upper airway obstructions. Hair loss and mental and psychiatric side effects including confusion, extreme emotional states, especially anxiety, vivid dreams, visual and auditory hallucinations, sleepiness, and effects on learning are other side effects of levodopa (Connelly & Fox, 2012). Levodopa causes fewer psychiatric side effects than other drugs including anticholinergics, selegiline, amantadine, and dopamine agonists. Psychiatric side effects often occur at night, therefore, some doctors recommend reducing the evening dose (Connelly & Fox, 2012).

Monoamine Oxidase B (MAO-B) inhibitors block monoamine oxidase B, an enzyme that degrades dopamine. Selegiline was commonly used in early onset disease in combination with L-dopa for maintenance (Brunton, Chabner, & Knollman, 2011). Concerns of the significant side effects have been raised. Azilect, a newer MAO-B Inhibitor, is used alone during early stage Parkinson’s disease and in combination with L-dopa for moderate to advanced Parkinson’s disease. Side effects of MAO-B inhibitors include orthostatic hypotension, hypertension if combined with drugs that increase serotonin levels, such as many antidepressants (Brunton, Chabner, & Knollman, 2011). A dangerous increase in blood pressure may occur if patients eat foods rich in the amino acid tyramine, while taking selegiline or rasagiline, and for two weeks after stopping the medications. Patients should avoid foods such as aged cheeses, processed lunch meats, pickled herring, yeast extracts, aged red wine, draft beers, sauerkraut, and soy sauce (Connelly & Fox, 2012).Parkinson’s Disease Precautions Essay Paper

Dopamine agonists stimulate dopamine receptors in the substantia nigra. Dopamine agonists are effective in delaying motor complications during the first years of treatment (Katzung, Mastes, & Trevor, 2012). Newer dopamine agonists, Mirapex (pramipexole) and Requip (ropinirol) are the most commonly prescribed. Mirapex appears to work better and have fewer side effects than requip. Side effects include nausea, vomiting, constipation, headache, nasal congestion, nightmares, hallucinations, and psychosis. Bromocriptine is the only ergot dopamine agonist approved for treatment in the US (Connelly & Fox, 2012). Apomorphine is a dopamine agonist used as a rescue drug in people having on-off effects severe enough to require going off L-dopa for a few days. Because it causes severe nausea and vomiting, it must be taken with an anti-emetic. Rotigotine (Neupro) is a once daily transdermal patch to treat early and advanced stage Parkinson’s disease (Connelly & Fox, 2012).

Catechol-O- Methyl Transferase Inhibitors (COMT Inhibitors) increase concentrations of existing dopamine in the brain. Entacapone (Comtan, Stalevo) is the current standard COMT inhibitor. It improves motor fluctuations related to weaning off effects. The side effects include involuntary muscle movement, confusion, hallucinations, nausea, vomiting, insomnia, headache, urinary retention, cramps, diarrhea, less common constipation, susceptibility to respiratory infection, sweating and dry mouth (Brunton, Chabner, & Knollman, 2011). A major concern is reports of death from liver damage in patients taking tolcapone (Tasmar) and is recommended only for patients unable to tolerate other drugs. Entacapone does not appear to have the same effects on the liver and does not require the same monitoring (Katzung, Mastes, & Trevor, 2012).Parkinson’s Disease Precautions Essay Paper

Anticholinergic drugs were the first used in the treatment for Parkinson’s disease. They are used only for control of tremors in early stages (Brunton, Chabner, & Knollman, 2011). Side effects are dry mouth, nausea, urinary retention, blurred vision, and constipation. They can increase heart rate and constipation. They may cause mental problems including memory loss, confusion, and hallucinations (Brunton, Chabner, & Knollman, 2011).

Amantadine stimulates the release of dopamine and may be used with early mild symptoms. Side effects include swollen ankles, and mottled skin, visual hallucinations. Overdose can cause serious and life-threatening toxicity (Brunton, Chabner, & Knollman, 2011).

Other movement disorders include cerebral palsy, ataxia, and Tourette syndrome. They happen when a change in the nervous system affects a person’s ability to move or stay still.

The National Institutes of Health (NIH) note that, in the United States, around 50,000 people receive a diagnosis of Parkinson’s disease each year, and around half a million people are living with the condition.

Read on to find out more about this condition, the early signs, and what causes it.

What is Parkinson’s disease?
Tremor in one hand is a early sign
Tremor in one hand is a early sign of Parkinson’s disease.
The symptoms of Parkinson’s disease develop gradually. They often start with a slight tremor in one hand and a feeling of stiffness in the body.Parkinson’s Disease Precautions Essay Paper

Parkinson’s disease (PD) is a progressive, neurological disease involving motor (e.g., bradykinesia, tremor, rigidity, and postural impairment) and nonmotor (e.g., depression, anxiety, sleep disorders, fatigue, dysautonomia, and pain) symptoms [1, 2]. Its symptom profile and progression differ between individuals. The core pathology believed to cause the main motor symptoms is a striatal dopamine deficit due to progressive loss of nigrostriatal dopaminergic neurons [2]. Symptomatic dopaminergic therapy is initially successful, but a fluctuating drug response and dyskinesias often develop after some years. With the occurrence and progression of both motor and nonmotor symptoms, often in complex and fluctuating patterns [1, 3], the disease is typically perceived as unpredictable and difficult to control [4].

An increasing number of studies have considered the consequences of PD characterized symptomatic profiles, relationships among symptoms, and the impact of various features of the disease from the perspective of persons living with PD [5–7]. Previous studies have reported how persons with PD (PwPD) experience various disease aspects, such as loss of motor control, walking difficulties, environmental influences, cognitive and executive dysfunctions, emotional reactions, sleep disorders, difficulties in managing activities of daily living, neuropsychiatric reactions, social withdrawal and isolation, communication difficulties, and loss of physical and psychosocial competence [8–13]. Collectively, these and other studies have provided important insights into several aspects of PD. However, available studies have typically focused on relatively specific aspects of the disease (e.g., communication, fatigue, and walking) or subgroups of PwPD, such as women and middle-aged or older people [14–17]. Few qualitative studies have attempted to capture the overall impact of PD on daily life, and available studies [18, 19] stem from the era before the introduction of, for example, modern dopamine agonists and enzyme inhibitors [20]. To the best of our knowledge, there are no studies that take a holistic approach when describing the consequences of living with PD. The aim of this study was therefore to explore the overall impact of living with PD.Parkinson’s Disease Precautions Essay Paper

2. Materials and Methods
2.1. Participants and Recruitment
Thirty consecutive Swedish-speaking people with clinically diagnosed PD from a Swedish movement disorder clinic were selected by purposeful sampling and invited to participate [21]. Specifically, we aimed to achieve variations regarding age, gender, disease duration, and PD severity. Exclusion criteria were ongoing psychiatric side effects from medication and clinically significant comorbidities that could compromise the ability to participate (e.g., dementia), as determined by a specialized PD nurse. Nineteen persons, 11 women and 8 men aged 55–84 (median: 66 years, q1–q3: 61–73 years), were able to participate and provided signed informed consent. They were diagnosed with PD since 3–27 years (median: 11 years, q1–q3: 7–14 years). Disease severity ranged from mild bilateral disease (Hoehn & Yahr stage II) to severe PD with inability to stand or walk unless aided (Hoehn & Yahr stage V) [22]. All participants were treated with levodopa, and additional antiparkinsonian therapy consisted of oral dopamine agonists (pramipexole and ropinirole), COMT inhibitors (entacapone and tolcapone), amantadine, subcutaneous apomorphine infusion, and deep brain stimulation. The study was conducted in accordance with the Declaration of Helsinki and was approved by the local research ethics committee.Parkinson’s Disease Precautions Essay Paper

2.2. Data Collection
Data were collected by means of face-to-face semistructured interviews, which were recorded and transcribed verbatim. The interviews lasted for 60 to 90 minutes and followed a preprepared interview guide. All interviews were conducted face to face in privacy, without the involvement of caregivers/family members. The interviewer started each interview with the phrase: “We are interested in learning more about how you have experienced the consequences of Parkinson’s disease, now and in the past. Could you please tell me how you first noticed the disease?,” followed by “Can you describe how the disease has influenced your daily life?.” The interview guide consisted of a checklist of areas that might potentially add to the understanding of the consequences of PD. The areas were: at home, at work, in personal relationships and social life, cognitive ability, personal care, leisure activities, sleep, and rest. If not covered spontaneously by the respondent, these areas were explored by open-ended questions. When needed, prompts were used to encourage respondents to explore and expand statements in greater depth.

2.3. Data Analysis
Following verbatim interview transcription, data were analysed as described by Graneheim and Lundman [23] and Patton [21], according to the following steps: (1) All interviews were read separately several times in order to get an understanding of the essence of each interview and to identify primary patterns in the data. (2) Meaning units were identified and (3) coded with regard to the content. (4) Clusters of aspects that emerged in the coded data were organised in subcategories. (5) Subcategories were sorted by their conceptual representation, ending up in four main categories, representing a more abstract level of understanding. To assist and organise the analysis, the OpenCode 4.0 software for qualitative analysis was used. OpenCode 4.0 is a software for coding and categorising qualitative interview or observational data. The program was originally developed for grounded theory and qualitative content analysis, but can be used with most qualitative methods [24].Parkinson’s Disease Precautions Essay Paper

3. Results
The impact of living with PD can be understood as “Changed prerequisites for managing day-to-day demands,” “Loss of identity and dignity,” “Compromised social participation,” and “The use of practical and psychological strategies” with internal variations seen as subcategories (Table 1).

Table 1: The impact of living with Parkinson’s disease.
3.1. Changed Prerequisites for Managing Day-to-Day Demands
The participants described how prerequisites for managing day-to-day demands had changed due to deteriorating physical, psychological, and cognitive functioning. This change affected most activities, which became difficult to manage, as some perceived their abilities to be severely affected or completely lost. The changed prerequisites concerned deteriorating physical functioning, fatigue, psychological changes, and mood swings as well as cognitive impairments.

Deteriorating physical functioning was evident in that the participants described that they had become slower no matter what they were doing and that everything took more time. Walking was more difficult because they felt stiff and it was increasingly hard to move the legs and feet. Walking pace had slowed down and keeping balance was more difficult. Fear of falling was common, and many had experienced several falls. They described that they sometimes suddenly could not move at all and felt like a statue, and there was nothing they could do about it.

I couldn’t walk any further than maybe out of the house and into the garden … then I found myself in a world that was totally my own … . I became completely stiff … my wife shouted at me that “you have to move”, but I was completely stuck … . (Participant 8)

Other physical changes included painful cramps and pain in general. In combination with deteriorating fine motor abilities, daily activities (e.g., chores, shopping, getting dressed/undressed, and taking care of personal hygiene) became time-consuming, difficult to perform, and physically and psychologically challenging.Parkinson’s Disease Precautions Essay Paper

It takes time to do the buttons … . It’s irritating sometimes. It takes a long time before you have finished dressing… . (Participant 10)

The participants described fatigue as an overwhelming and general feeling of tiredness and loss of energy. A sense of feeling completely worn-out and unable to take action could appear suddenly and at any time. Most of the time nothing could be done to solve the situation except to go to bed. Fatigue was also described as being both physical and psychological.

I become so … utterly worn out. I can’t hang my clothes… , put the dishes away. I can barely find the strength to go to the bathroom, or brush my teeth, because nothing works, you see. I just get slow, indifferent … . I don’t care about anything but to go to bed … and just lie down… . (Participant 1)

Psychological changes and mood swings were typically perceived as being related to physical deterioration and were described as difficult to control, for example, a sense of panic and powerlessness. Participants worried about the future and about what would happen when they could no longer care for themselves. Thoughts like these brought about anxiety and fear. Some felt depressed and downhearted most of the day, sad at being disabled, alone, and unable to do what they wanted to do. These thoughts could become destructive and murky, and some had feelings of wanting to die; what was the point of staying alive when life itself offered so little?

… maybe … . I need help to look back on my life … Well to … to be able to see the meaning of life … to shed some light over this darkness … . To go on living or not … there are … there are days when I feel that everything is really bad and … there is no point in anything … . (Participant 15)Parkinson’s Disease Precautions Essay Paper

Participants described how cognitive impairments were manifested, for example, problems in remembering and concentrating. Those who used to read a lot found it difficult to remember what they just read and to understand the context. Communicating with others was difficult as names were often forgotten, and what to say and finding the right words became even worse when they were nervous. It became difficult to do things that they used to do, for example, cooking or carpentry as the ability to count and measure was compromised. They described problems organising and keeping papers and other things in order; it felt like the brain was in a state of chaos.

It’s just like I … . I become indifferent … to some things. Very hard to keep things in order … [laughs]. I move things from one place to the other and I think that I have put everything right and then everything is … . There’s some … there’s some disorder … some chaos in the brain… . (Participant 1)

3.2. Loss of Identity and Dignity
As the disease progressed, dependency on help with practical matters increased and family relationships changed. Participants expressed bitterness and shame of the person they had become and tried to conceal the disease. They noticed that the physical and mental changes affected their self-esteem, as well as how they were perceived by others. They felt humiliated and less confident when judged by others. Loss of identity and dignity altered family relationships, gave a sense of lost identity, and a sense of being worthless.

Altered family relationships involved affected the bond between husband and wife. Some described that their partner was afraid of future demands and responsibilities and was away more often. As the illness progressed, some families decided to redistribute household and family responsibilities. They found it difficult to ask for help as they wanted their families to treat them as they used to, without showing any special considerations. Participants became more dependent on practical help from their family members, for example, cooking and other chores, but also their personal hygiene and getting dressed, as well as concerns regarding their personal safety.Parkinson’s Disease Precautions Essay Paper

Well, I think that it feels very bad … needing to ask for help … to get dressed … and again when I want to go to bed … and at the same time one becomes really frightened … if I was alone in the house, what was I supposed to do … and imagining things like … . There is nobody here, what if I were to fall … . (Participant 8)

A sense of lost identity was described by all participants. Although they felt that deep inside they were still the same person, they were also aware that they were physically changing. The posture became more stooped, their faces looked more tired, and they were not as fast and skilled as they once were. They could have held positions in management and family responsibilities, a person that others would seek advice from and see up to. Now, they had to give up doing things or taking responsibilities, both at home and at work. They found themselves being dependent on others. This made them feel belittled, insecure, and less confident, as if they no longer belonged to this world. They felt themselves to be a professional and a personal failure, something that deprived them of their self-image and identity.

… well, then you become sort of powerless … and indecisive … . You can’t decide … you can’t make up your mind… . (Participant 5)

A sense of being deprived of one’s self-worth could appear when meeting with others. It made them feel uncomfortable and resented if they felt that someone pitied and felt sorry for them. They wanted to be treated as a valid citizen although they had PD, just like they had been treated before the diagnosis. Some also worried that they would be taken for an alcoholic due to physical symptoms such as balance problems and tremor. They noticed that people sometimes stared or looked at them in an odd way, and they also felt exposed to naive and hurtful comments.Parkinson’s Disease Precautions Essay Paper

Although I have Parkinson’s disease, I want to be respected. I want to be able to do … take care of things like I always did in the past and I want to take an active part in society … hmmm … and I don’t want to be looked down upon in any way … I want to be accepted even though I do have Parkinson’s. (Participant 15)

3.3. Compromised Social Participation
The prerequisites for taking part in social activities had changed and affected all aspects of their social life. They felt increasingly socially isolated, which in part was due to feeling embarrassed of their changed persona. In addition, some had speech problems, which made communicating difficult. Compromised social participation had to do with limited ability to meet with others, feeling socially isolated, social embarrassment, and speech problems.

Limited ability to meet with others and decreased activities in daily life were common. Not being able to drive was problematic as it made it more difficult to get around. Using public transportation required planning and was regarded as inconvenient. Other activities that were affected were holding cards whilst playing bridge, outings in the countryside, riding, playing football, or going out dancing. It was also difficult to manage stairs, to go in and out of shops, do the shopping, and other daily activities.

And when one needs to go into shops, which rarely happens, it’s not easy when there is a flight of stairs that has to be managed. (Participant 10)

Feeling socially isolated and being alone was hard. Even if it sometimes was preferable to be alone, there was also a feeling of being avoided, even by close friends. Participants often wished something would happen to break the silence of their secluded life, for example, a phone call or a letter. Even if there was only a bill it was read thoroughly as a strategy to feel connected to the outer world.Parkinson’s Disease Precautions Essay Paper

… well, from the moment I have the letter in my hand, I open it and it … it … just by doing that, it’s something that makes you feel more alive … because it’s a moment that feels exciting … . What’s inside the envelope, what does the letter say … and then you start reading it … and if it’s a bill I start to take an interest to it … you make as much of it as possible … in order to … live on… . (Participant 9)

The participants described social embarrassments as their facial expressions and nonverbal communication were reduced. Involuntary movements were a problem, for example, when having dinner with family and friends. Glasses and cups could suddenly be knocked over, tremors made it difficult to use cutlery and handling food or drink. Eating was time-consuming, and they felt embarrassed by keeping others waiting. They felt bitter at having the disease, which made them try to hide their symptoms.

It was like … when I had customers … and they sort of … why do you walk so funny? And then I … oh, it’s just because one of my toes is hurting … or something like that … hmm … that’s how I kept it hidden for … well … at least … certainly for ten years… . (Participant 8)

Speech problems were frustrating to the point where some stopped talking altogether, and others found it difficult to articulate. Being nervous or stressed tended to make it worse. These problems could make it impossible to speak on the phone, and consequently people stopped calling.

… they told my children … to tell me that … that … we … we … we … don’t understand what he’s saying so there is no point calling … . And I understand that … . I find it equally … equally embarrassing… . (Participant 9)Parkinson’s Disease Precautions Essay Paper

3.4. The Use of Practical and Psychological Strategies
The participants used different strategies to adapt to various situations. Trying to find practical solutions were most common, for example, seeking information, planning, and using aids. Other examples of strategies used to promote psychological well-being were to have a positive attitude or to compare one’s own situation to that of others. Practical and psychological strategies used were to be able to foresee and plan, to compensate for lost functioning, trying to maintain a positive attitude, using downward comparisons, and accepting support from health care.

To be foreseeing and plan was necessary when managing everyday life. Most things took more time, and those with cognitive difficulties needed detailed planning, taking notes, and doing things step-by-step. Medication required a great deal of planning and most participants followed a schedule. Even though all precautions were taken, it was still uncertain if they would manage to go through with their plans due to the unpredictability of the disease. They felt embarrassed when they had to cancel at the last minute.

… I don’t always make plans just for myself. Sometimes there are others involved and it feels really bad to always be the one who cancels … for example if we’re going to the movies or something… . (Participant 5)

Various compensatory strategies were applied to compensate for lost functioning, for example, doing chores sitting down instead of standing up or to avoid reaching for things. Several situations were avoided altogether to minimise the risk of falling and being injured, for example, to shower instead of taking a bath. Some also chose to pay for the services that they were unable to do, for example, cooking and cleaning.Parkinson’s Disease Precautions Essay Paper

Well, I … eh … I … eh … do the dishes, when I’ve finished eating … for other chores like cleaning up, I’ve help from others … hired help … and my children they cook … when they cook for themselves, they also cook for me and then they freeze the food and bring it to me. I can take care of my personal hygiene. I take a shower every morning, but … eh … to take a bath, which I used to love doing … it’s not possible anymore. I can’t get out of the bathtub. (Participant 9)

Trying to maintain a positive attitude was used to feel psychologically better, for example, trying to be optimistic, not to worry, enjoying the moment, making the best of the situation, trying to live life as normally as possible, and pushing all thoughts of the future aside. PD could progress in so many ways that they found it best to settle for what little they had and make the most of every moment. Some described the importance of fighting back and not giving up. For example, thinking of children and grandchildren was also helpful in finding enough strength to keep on living.

I have to start from how it is … and make the best of the situation … and so far, that’s worked. It’s not really a disaster to be ill … . Because you become sort of … you look at life differently and become more grateful… . (Participant 14)

The participants were using downward comparisons, comparing themselves with those worse off, for example, while attending support group meetings. This strategy was helpful in realising that they still functioned relatively well, given the circumstances. However, others described the opposite reaction as it could make them worried and anxious that they might end up in a similar situation.

Well, of course you compare yourself with others … . You make certain comparisons with … well, if you are sitting down … having a conversation with someone, you tell yourself … well, the things that he’s doing aren’t something that I do … you sort of compare yourself with that person … and then you choose to look at the best parts of the situation, and I tell myself that I’m much better off than he is… . (Participant 8)Parkinson’s Disease Precautions Essay Paper

The participants also used self-deception, that is, convincing themselves that things were not as bad as they might seem. Regardless of the individual’s specific strategy, it was about finding a way that worked, to adapt and try to accept the situation.

Accepting healthcare support was important in managing the situation, even if accessibility was an issue. They wished that it would be possible to have one person to turn to for support and felt that the time between scheduled clinic visits was too long.

Over time, other symptoms develop, and some people will have dementia.

Most of the symptoms result from a fall in dopamine levels in the brain.

One study, based in France, found in 2015 that men are 50 percent more likely to develop Parkinson’s disease than women overall, but the risk for women appears to increase with age.

Early signs
Here are some early signs of Parkinson’s disease:

What is REM sleep behavior disorder (RBD)?
What is REM sleep behavior disorder (RBD)?
What is REM sleep disorder? Click here to find out more.
READ NOW
The importance of recognizing early symptoms
Many people think that the early signs of Parkinson’s are normal signs of aging. For this reason, they may not seek help.

However, treatment is more likely to be effective if a person takes it early in the development of Parkinson’s disease. For this reason, it is important to get an early diagnosis if possible.

If treatment does not start until the person has clear symptoms, it will not be as effective.

Moreover, a number of other conditions can have similar symptoms.

These include:Parkinson’s Disease Precautions Essay Paper

drug-induced Parkinsonism
head trauma
encephalitis
stroke
Lewy body dementia
corticobasal degeneration
multiple system atrophy
progressive supranuclear palsy
The similarity to other conditions can make it hard for doctors to diagnose Parkinson’s disease in the early stages.

Movement symptoms may start on one side of the body and gradually affect both sides. Parkinson’s Disease Precautions Essay Paper