Analysis of the Causes and Treatment of Parkinsons Disease in a Patient - Essay Example

? of Lecturer] Analysis of the Causes and Treatment of Parkinson’s Disease in a Patient Introduction This essay is a summary report following a research conducted about Parkinson’s disease (PD). It is divided into various sub sections to allow a detailed discussion. The first section defines what Parkinson’s disease is, when it was first discovered, who had it first and whether it is a disease of both sexes. Also discussed are the signs and symptoms that come with it. The second section deals with diagnosis, treatment and management of PD. There is a detailed discussion of the pharmacological and non pharmacological measures taken to manage PD, and the long term care that should be given to patients suffering from the disease. The last section is a conclusion based on the matters discussed in the essay and basically summarizes the facts of the research and projects the future prospects of the disease. Parkinson’s Disease Parkinson’s disease (PD), or primary Parkinsonism, is a medical term that refers to a progressive neurological condition that affects the central nervous system. PD is the second most common neurodegenerative disease after Alzheimer’s and comes with a lot of burden on patients and their families as well. Patients suffering from PD are associated with disability, increased morbidity and lower life expectancy than the rest of the population Adler 27). This condition is believed to be caused by the death of cells that generate dopamine found in a region of the midbrain called substantia nigra. A 2005 literature review put the estimates of incidences of the disease at between 12 and 26 per 100000 individuals and the prevalence at around 130 in every 100,000. PD itself does not pose immediate threat to an individual. However, individuals that have borne it for a long time are susceptible to physical and mental illnesses that can lead to death (Schapira et al 1092). The disease was first discovered in 1817 by an English physician, Dr. James Parkinson. In an article titled ‘An Essay on the Shaking Palsy’, he described in detail, a disease that progressed with time and was characterised by abnormal posture and gait, resting tremor, reduced muscle strength and paralysis (Asenbaum et al 1215). Modern medical practice divides the symptoms of this disease into early and later stage symptoms. Early stage symptoms associated with PD are usually movement-related and include slow movement, rigidity, shaking, gait and difficulty while walking. Later on in the advanced stages of the disease, behavioural and thinking problems arise. These symptoms include neuropsychiatric disturbances like depression, apathy, hallucinations, anxiety disorders, fatigue, sleep disorders, hypophonia, poor bowel movement, drenching, sweats, pain, sexual dysfunction, dementia, depression, and sialorrhoea (Adler 9). Other symptoms are sensory and emotional. PD is a disease common among older people, with the onset age at about 50 years (Mylne et al 1015). The Central Nervous System Since PD is a disease of the central nervous system (CNS), it is important to have a basic idea of CNS’s structure and functioning. The CNS refers to the part of the nervous system that consists of the brain and the spinal cord, with the brain in the cranial cavity and is protected by the skull and the spinal cord lies in the spinal cavity and is protected by the vertebrae. Its function is to integrate all the information sent to it from other parts of the body and use this information to coordinate the proper functioning of the body. It works hand in hand with the peripheral nervous system to control behavior. The basic structure of the CNS is the neurone. Together with neurotransmitters, they are fundamental in relying information throughout the CNS in the form of electric pulses. When a disease of the CNs such as PD attacks an individual, it leads to a deformation of the structure of neurones causing them to malfunction. This results in abnormal functioning of the CNS causing the symptoms of PD such as rest tremor, slow movement and rigidity. Causes of PD The main cause of PD in a number of cases is attributed to genetic factors although in majority of people it remains unknown. Other factors have also been associated with Pd though no causal relationships have been established. These include head injuries, exposure to pesticides and a people’s lifestyle that may involve consumption of contaminated drinking water and foodstuff. Proponents of this school of thought argue that cumulative consumption of insecticides such as chlorpyrifos and pesticides such as rotenone pose individuals to risk of acquiring PD since these substances accumulate in this substantia nigra research in this line is still underway and therefore the correctness of this theory cannot be verified (Marieb et al 115). Scientific research indicates the PD is a genetic disorder because mutation of specific genes result in PD. Research shows that 5% of the human population has shown forms of the disease caused by a mutation of one of many specific genes. These are the genes that code for parkin (PRKN), ATP13A2, leucine-rich repeat kinase 2 (LRRK2 similarly called dardarin), alpha-synuclein (SNCA), PTEN-induced putative kinase 1 (PINK1) and DJ-1. SNCA is trivial in PD development since the Alpha-Synuclein protein is the main constituent of Lewy bodies. A mutation of the gene that involves change of only a single nucleotide change, and further multiplication of the locus containing it has been found in separate groups in cases of familial PD. Research further shows that LRRK2 mutations are the major cause of random and familial PD, accounting for as much as 5% of all cases of familial PD and 3% of random PD. Epidemiology of PD Parkinson’s disease is second only to Alzheimer’s among neurodegenerative disorders. It currently affects 7 million people globally with a prevalence of about 0.3% of the population in industrialised countries. PD is a common disease among the elderly, with research putting the prevalence at 1% and 4% in those over 60 and 80 years respectively. The onset age varies around 60 years though cases of the disease have been reported in people as young as 20. Though disputed, research indicates that PD is less prevalent among those of African and Asian ancestry and is more common in men than women (Mylne et al 12). A lot of risk factors and possible solutions have been proposed in relation to the modes of spread of the disease though none has been experimentally proven. Research into this field has yielded faulty and contradictory results, case in point being the proposed increased risk factor on exposure to insecticides. Diagnosis, Treatment and Management of PD The diagnosis and management of PD can be a challenge owing to the fact that it shares several symptoms with a host of other neurological diseases. The United Kingdom Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria and Dopamine Transporter/Single-Photon Emission Computed Tomography (Dat-SPECT) are diagnostic tools that are used to improve the accuracy of the tests. Management of PD is shifting towards early treatment because research has indicated that patients who start receiving medication in the early stages have a higher chance of recovery (Pahwa et al 5). Since there are no conclusive tests to accurately diagnose PD, the process relies on the experience and skills of the physician, signs and symptoms and response of the patient to the medication administered. The basic diagnosis criteria for PD involve the presence of two of three fundamental features. These are bradykinesia, rest tremor and rigidity. Another important test may include an improvement of symptoms with levodopa. The main setback with this criteria for diagnosis is that it results in a large number of patients with atypical Parkinsonism being falsely diagnosed with PD (Suchowersky et al 970). The United Kingdom Parkinson’s Disease Society Brain Bank Clinical Diagnostic Criteria (UK PD Brain Bank criteria) offers more specific criteria for testing for PD. They are commonly considered the reference diagnostic criteria for PD. This criterion involves a three step process. The first step involves identification of signs and symptoms that are required to diagnose Parkinsonism. It is followed by a second step that involves checking for sign and symptoms that will exclude a diagnosis of PD. The third and final step is concerned with identification of criteria to support the diagnosis of PD (Schrag et al 540). Bank Clinical Diagnostic Criteria for PD As stated before, the first step involves diagnosis of parkinsonian syndrome. It includes a test for Bradkynesia, which refers to slowness in initiation of voluntary movement and a progressive reduction in amplitude and speed of repetitive tasks. It also involves a test of one of the following: 4-6Hz rest tremor, muscular rigidity and postural instability that is not initiated by vestibular or proprioceptive dysfunction. The second stage that tests for exclusion of PD checks for a history of repeated strokes with a steady progression of features of parkinsonism, it also checks for oculogyric crises, family history incase of affected relatives , early severe autonomic involvement and negative response to doses big doses of levodopa (Hauser et al 563). Onset of treatment is recommended if a patient exhibits these symptoms. The last stage deals with tests to support diagnosis of PD. It checks for progressive disorder, rest tremor, excellent response to levodopa and persistent asymmetry affecting the side of onset most. Differential Diagnosis of Parkinson’s Disease Differential diagnosis of Pd is a challenge owing to the large number of neurological diseases that have exhibit the same features as PD. In order to clearly diagnose PD, the UK PD Brain Bank criteria and Dat-SPECT are used to clearly differentiate PD from other forms of Parkinsonism and other diseases of the central nervous system. Treatment and Management of PD The main aim of the initial treatment for PD is to use as little drugs as possible to control the symptoms without causing severe effects. There are several factors that affect the decision to initiate treatment, and which mode of treatment to be used. These factors include co-morbidity, psychiatric and cognitive issues, symptom severity, lifestyle and employment. Initial medication options include non pharmacological treatment, while in the advanced stages drug use is inevitable. Non-Pharmacological Treatment Research in both humans and animals has shown that physical therapy and targeted exercise early in the course of the disease can provide health benefits as well as protect the nervous system. In view of this, it is imperative that all PD patients adopt an exercise plan or have a qualified physician draw up one for them. The patient should not be limited to exercises that target only the limbs but also other forms of exercise meant for the improvement of speech and swallowing (Russell et al 7). These exercises should be initiated long before serious problems set in (Hirsch et al 230). It is also important for patients and those surrounding the patient to receive proper education on Pd and also enlist themselves as members of a support system such as a PD support group. Other aspects of non pharmacological treatment involve the patient having a healthy diet and adopting recommended sleep habits. Pharmacological Treatment In the advanced stages of the disease, use of surgery, medications and multidisciplinary management is inevitable to relieve the symptoms of PD (Kieburtz 39). The groups of drugs commonly used to relieve motor symptoms are monoamine oxidase inhibitor (MAO-B), dopamine agnostics and levodopa. The stage of the disease also determines the group of drugs is to be used on the patient. The first stage refers to when a patient has already developed disability for which he or she needs pharmacological intervention, and a second stage during which an individual exhibits complications related to the use of levodopa. The initial stage of treatment will try to control the symptoms and side effects that result from improvement of dopaminergic functions (Benamer et al 980). The latter stage of treatment aims at reducing symptoms while controlling the variations of the patient’s response to medication. The physician must also be ready to manage unexpected withdrawals from and overuse of medication. In instances when use of medication is not enough, doctors may resort to deep brain stimulation and surgery (Brooks 249). The following section looks at the groups of drugs used in the management of PD. Levodopa/Carbidopa Levodopa/Carbidopa is the most effective treatment for PD and has also been the longest in use, spanning over 30 years. It is required by all patients at some point in the course of the disease. However, in large doses and prolonged use it results in dyskinesia and motor fluctuations (Witjas et al 409). Earlier Versus Later Levodopa Therapy in Parkinson’s Disease (ELLDOPA) studies have showed improved UPDRS motor scores for patient that are subjected to levodopa medication than those on placebo. Based on these results, it is recommended that when using levodopa for initial treatment, daily dosages should be kept to a below 600 mg and additional medication may only be added if it necessitates. Carbidopa use has been associated with side effects such as dizziness, vomiting, nausea, motor fluctuations, orthostatic hypotension and dyskinesia. It is important to note that levodopa is not recommended for initial treatment of PD (Stocchi et al 20) MAO-B Inhibitors Monoamine Oxidase Inhibitors (MAO-B Inhibitors) work on the mechanism of blocking MAO-B and allowing more dopamine to reach the brain. Examples of these inhibitors currently in use are rasagiline and selegiline. Research findings suggest that rasagiline has a very mild effect in the early stages of the disease. However, as the disease progresses, it has a more pronounced effect on the signs and symptoms of PD (Olanow et al 70). Research further shows that selegiline contains amphetamine metabolites that cause hallucinations, confusions and insomnia (Palhagen et al 1205). Rasagiline on the other hand is metabolised to aminoindan and is well tolerated by the body. Use of MAO-B inhibitors is recommended in patients with mild symptoms and levodopa or a dopamine agnostic is added as the symptoms get more severe (Lang 949). Dopamine Agonists These are substances that bind to the dopaminergic post –synaptic dopamine receptors of the brain and have effects similar to those of levodopa. They are currently used for initial therapy to delay motor complications in patients that have displayed early motor symptoms. Dopaminergic agnostics include lisuride, bromocriptine, ropinirole pergolide, pramipexole, piribedil, apomorphine, and cabergoline. The most commonly used of these are ropinirole and pramipexole, with improvements as much as 4-5 points score above placebo in the UPDRS total score. The common side effects involving the use of dopamine agnostics include confusion, hallucinations, constipation, memory loss, urinary retention and blurred vision. It is because of these side effects that the use of dopamine agnostics should be avoided in older patients. Conclusion Accurate diagnosis of PD is difficult and requires a skilled and experienced physician using the UK PD Brain Bank criteria and the Dat-SPECT to improve the accuracy of the test. Modern measures of managing PD should include initiating both non pharmacologic and pharmacologic therapy much earlier before the symptoms get out of control. As part of the treatment, patient should be advised to exercise regularly as well as adopt other healthy lifestyle habits to improve their quality of life. The choice of treatment however depends on an individual’s present state. The early treatment options available include dopamine agnostics, levodopa, MAO-B and rarely amantadine. The best way forward to deal with PD now and in the future is to initiate non-pharmacological treatment as soon as a patient is correctly diagnosed, if there is no apparent disability then MAO-B should be initiated. As symptoms progress, younger patients below 70 years should be given a dopamine agonist while those above 70 years should be given controlled dosages of levodopa. Depending on the lifestyle of the patient, for instance a younger patient still in employment, levodopa rather than a dopamine should be given in order to maintain a desired level of functioning. 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