Parkinson’s disease (PD) is a long term, chronic and progressive disorder of the body’s immune system which majorly affects the motor system hence making mobility difficult. PD develops slowly from something as negligible a tremor on your arms (Sharma, 2008). The essay below tries to elaborate on the cause and potential treatments of the disease. The social implications of PD are also discussed (Sharma, 2008).
Parkinson’s disease has no known specific causal factor. It is believed that it may be a combination of both genetic and/or environmental factors. Thus, the cause would vary from person to person depending on the individual’s current family background and the environmental factors they interact with in a daily basis (Rajesh Pahwa., 2009). Research studies have shown that there is an at least 9% possibility of a person developing PD if they have a close relative who has the disease (Manfredsson, Okun and Mandel, 2009). Research has also revealed that various gene mutations during a person young age also increase the chance of developing the disease. The affected genes include parkin, glucocerebrosidase, PINK-1 among others. Other researchers think that the cause of PD is environmental. Exposure to toxins, illness, head trauma and injuries are believed to cause the disease.
There is less risk among tobacco smokers and in people who regularly take coffee or tea. Exposure to toxins such as the insecticide permethrin, the herbicide paraquat and even agent orange is often associated with higher chances of developing PD. MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) is also another toxin that is associated with PD. It is believed that it can cause immediate and permanent parkinsonism because it reaches the brain it is converted into MPP+ which then kills neurons responsible for dopamine production PD cases of this kind are also rare (Rajesh Pahwa., 2009). It is not conclusive that contact will guarantee PD development as the evidence is not conclusive. However, both factors contribute greatly towards offering valuable clues in the PD research. Another factor is age. After Alzheimer’s it is the second most common age related neurodegenerative disease. The risk is higher amongst the older generation of people aged 60 and above (Rajesh Pahwa., 2009).
PD occurs due to the death of brain cells that produce dopamine. These cells are found in the mid brain in a region called the substantia nigra pars compacta. The cause of the death of the brain cells is not known but it is believed the growth of proteins into Lewy bodies in the neurons is involved in this. This dopaminergic differentiation in the basal ganglia results in motor impairment and difficulty. This is because the basal ganglion is responsible for smooth coordination of muscle movements. The accumulation of these Lewy bodies also occurs I other parts of the brain and body. The olfactory neurons are affected by these Lewy bodies resulting in a loss of sense of smell among PD patients.
Other dopamine producing cells are also found in the intestines and if they are affected it leads to gastro-intestinal disorders. Dopamine is a key neurotransmitter in this process as it increases effect of nerve impulses to the brain. Thus, when there is dopamine deficiency in the body the basal ganglia cannot necessitate smooth movement and coordination resulting in tremors, sluggish movement and lack of coordination. Often PD symptoms are not experienced until 80% percent of the dopamine producing cells is destroyed due to counter processes the brain may have to avert this.
Most common signs and symptoms of PD are motor related. Although current research has led to scientists also urging that non-motor related signs and symptoms are given utmost importance. The major motor symptoms are:
- Resting tremor- occurs in the early stages of the disease whereby a person experiences a slight tremor on an arm or leg on side of the body. As PD progresses the tremor may also be experienced on the other arm or leg.
- Bradykinesia- this is defined by slow movement. It results in inability to perform spontaneous movements. It also makes it harder to performing repetitive movements like tapping one’s feet. it may also cause difficulty in speech with patients having inaudible voices
- Rigidity- PD causes the muscles to be stiff. This means that they do not relax effectively hence decreasing the range of mobility a person has. Patients experience inflexibility in the limbs, trunk and neck.
- Postural instability – PD patients commonly tend to be unbalanced whenever standing. This is because they lack the necessary reflexes needed to maintain their posture. They can easily fall backwards if they are jostled or pushed.
The non-motor symptoms on the other hand include:
- Mood disorders such as depression and irritability
- Cognitive symptoms like slow thought, dementia, short attention span, memory difficulty
- Orthostatic hypotension especially when standing
- Sleep disorders like insomnia, rapid eye movement behavior disorder (RBD) or excessive daytime sleepiness.
- Loss of sense of smell
- Inaudible voices
- Impulse control disorders that cause patients to have compulsive habits such as gambling or shopping.
Other symptoms of PD are such as: drooling, fatigue, small handwriting, prolonged muscle contractions, loss of facial expression, constipation, and urinary inconsistence or retention (Shin, Pohlig and Habermann, 2016).
PD has no known cure. However, there are medications that can be administered to alleviate the symptoms of the disease. The main approach towards Parkinson disease medication is dopamine replacement therapy. The approach involves increasing dopamine levels or generally substituting for dopamine. Medication is often very effective in the short term but their effectiveness fades with time though at this point the symptoms are fairly controllable (Almeida and Hyson, 2008). The most effective is Carbidopa-levodopa. Levodopa is a naturally occurring chemical that can be converted to dopamine once it reaches the brain. Carbidopa on the other hand is used to increase efficiency by preventing premature conversion of levodopa. Its side effects are nausea, orthostatic hypotension and dyskinesia (in case of higher doses). This medication however wanes after years as its effectiveness tends to wear off (Almeida and Hyson, 2008).
The other form of treatment is dopamine agonists. Unlike carbidopa-levodopa, dopamine agonists copy the effect of dopamine on the brain and they also last longer. They directly stimulate the postsynaptic dopamine receptors to release an antiparkinsonian effect. They include pramipexole (Mirapex), apomorphine (Apokyn) and ropinirole (Requip). It has side effects such as hallucinations, sleepiness, and compulsive behaviors such as gambling and hyper sexuality. Third are MAO-B inhibitors which prevent metabolism of brain dopamine by the enzyme monoamine oxidase (MAO-B). They include selegiline (eldepryl) and safinamide (xadago) among others. Side effects are nausea insomnia and at times hallucinations.
The fourth class of medications is the Catechol-O-methyltransferase (COMT) inhibitors. They work by preventing the breakdown of dopamine in the brain and in so doing prolong the effects of levodopa. The side effects are dyskinesia and in the case of administering Tolcapone (tasmar) there is a risk of liver damage and liver failure. Other forms of medication are anticholinergics and amantadine. Side effects are hallucinations, constipation, memory impairment ankle swelling and purple mottling of the skin (Almeida and Hyson, 2008). Surgical procedures such as deep brain stimulation can be used where electrodes are implanted on parts of your brain to alleviate PD symptoms.
The prognosis of PD can be plotted down as a progressive neurodegenerative disease with no cure. It starts with unilateral symptoms that eventually become bilateral (Weinstock, 2016). Then there is a period of around 2-4 years where dopamine agonists are the main form of medication. After 5 years levodopa effectiveness begins to drop with motor complications like dyskinesia developing. After a few more years the dyskinesia will worsen and include falling, dementia and freezing which seriously impedes mobility. The course varies among patients but slow progression is characterized by tremor predominance. Monitoring of patients should be every 4 months by specialists. Patients are advised to avoid activities such as driving, engage in regular exercise and draft up a symptom journal so as to be able to maintain the motor related symptoms more sufficiently (Weinstock, 2016).
PD will have various implications on the patient such as: the change of social roles whereby due to their inability to perform various tasks because of their tremors other members of the family step up to fill in their role; lowered self-esteem causes patients social ties to grow smaller especially with their slow disoriented speech making socializing difficult; depression and dementia may set in making communicating and cooperating with the patients difficult; altered or ended could cause depression amongst patients; the side effects of medication that cause compulsive behaviors that may lead to addictions such as gambling; and the premature end of careers since patients have to relinquish their jobs because of PD (Grosset, Fernandez and Okun, 2009). Depression may also arise from social stigma from people who may misunderstand PD patients as being hostile or insane (Alterescu, 2012). The implications include financial strain to purchase appropriate medication and related therapy; worsened family relationships that could even lead to divorces; emotional distress such as anxiety and stress caused by the fear and uncertainty surrounding the ill family members future; social stigma associated with incorrect perceptions about PD. Psychological effects of PD include: anxiety and depression; anxiety due to uncertainty of their futures; and stress (The Michael J. Fox Foundation for Parkinson’s Research | Parkinson’s Disease, 2017).
In conclusion, Parkinson’s disease is a disease that should be made more aware. More research should also be done to shed light on the many things yet to be understood about it. Doctors recommend lifestyle changes and exercising regularly as a way of preventing the disease as well as alleviating the symptoms of the disease.
- Alterescu, K. (2012). Facial emotional expression following voice treatments in individuals with Parkinson’s disease.
- Grosset, D., Fernandez, H. and Okun, M. (2009). Parkinson’s Disease. London: Manson Pub.
- Shin, J., Pohlig, R. and Habermann, B. (2016). Self-Reported Symptoms of Parkinson’s disease by Sex and Disease Duration. Western Journal of Nursing Research.
- The Michael J. Fox Foundation for Parkinson’s Research | Parkinson’s Disease. (2017). The Michael J. Fox Foundation for Parkinson’s Research. [Online] Available at: http://www.michaeljfox.org [Accessed 21 Aug. 2017].
- Almeida, Q. and Hyson, H. (2008). The Evolution of Pharmacological Treatment for Parkinson’s disease. Recent Patents on CNS Drug Discovery, 3(1), pp.50-54.
- Weinstock, B. (2016). Preventing Parkinsons. Journal of Alzheimer’s Disease & Parkinsonism, 06(06).
- Sharma, N. (2008). Parkinson’s disease. Westport, Conn.: Greenwood Press.
- Manfredsson, F., Okun, M. and Mandel, R. (2009). Gene Therapy for Neurological Disorders: Challenges and Future Prospects for the Use of Growth Factors for the Treatment of Parkinsons Disease. Current Gene Therapy, 9(5), pp. 375-388.
- Rajesh Pahwa. (2009). Parkinson’s Disease. Oxford University Press, USA.