Parkinson’s disease (PD) is one of the neurodegenerative disorder associated with old age and is believed to be second in degree after Alzheimer’s disease (Alexander, 2004). PD is further known as the common severe movement disorder globally and affects about 1 percent of all adults over the age of 60 percent. In the US, approximately 500, 000 individuals have been reported to have PD, and its degree is mostly forecasted to triple in the following 50 years with the rapidly rising population. The disease affects about 7 million people across the world and one million in the US. De Lau & Breteler (2006), claim that PD is a slowly progressive neurodegenerative disorder that has not the precise or identifiable cause. Parkinsonism is further employed for the symptoms where etiology is recognized, for instance, parkinsonian symptoms as a result of toxic agents, strokes, infections, neuroleptic drug. Pathologically, PD is evidently defined by the discriminatory deterioration of the dopaminergic neuron at substantia nigra pars compacta in addition to the recurrent occurrences of ubiquitin-positive eosinophilic intracytoplasmic inclusion, commonly referred to as Lewy bodies, in the remaining neurons.
PD’s epidemiology arguably plays a critical role in the healthcare and is often utilized as one of the most suitable tools in the determination and examination of potential causes of PD. Analytical epidemiology helps in identifying risk factors which might be useful in leading to hints for causal agents of illness (De Lau & Breteler, 2006). Through the provision of the profile of disease parameters, including mortality, prevalence, and incidence, the descriptive epidemiology, on the other hand, is essential in the illustration and etiological examination of the disease. PD’s crude prevalence seems to vary significantly from 15 per 100,000 populations in China to about 657 in Argentina and from 100 to 250 in Europe and North America. The proportion within a particular time is approximately 0.3 percent in the industrialized economies (Alexander, 2004).
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PD has been reported to be higher among the elderly, and the rates tend to have risen from about one percent among the over 60 years of age to around four percent of the entire population above 80 (Smith & Kieval, 2000). The onset’s mean age of PD is about 60 years; however, 5-10% of cases apparently grouped as young onset PD, starts between 20-50 years. Despite the fact that gender differences seem to reveal the higher level of variability compared to association with increasing age, PD is seemingly common among men than women, and this tends to range from a 1.2:1 ratio up to a 1.5:1 ratio.
Other studies have shown that PD is prevalent among the men than women. The emerging cases of PD are roughly 8 and 18 per 100,000 person-years. Based on the ethnic distribution, research has shown that the white in North American and Europe have higher prevalence rates of about 100 to 350 per 100,000 populations (Smith & Kieval, 2000). The Blacks, China, and the Asians have the lowest rates, roughly one-fifth to one-tenth of whites. Geographic variations have further been reported concerning PD where the crude prevalence is about 657 per 100,000 in Argentina, 15 per 100,000 in China, 131 per 100,000 in Mississippi, USA and 328 per 100,000 in India. In the US, the average yearly age-adjusted deaths related to PD was reported in 1962, and 1984 was about two deaths per 100,000 for the whites men and one for the nonwhite men, one death per 100,000 for the white women, and less than one death per 100,000 for the nonwhite women. The number of deaths tends to increase significantly for individuals of ages 75 years and older; however, it drops considerably to those below the age 70.
Normal Physiology of the System Involved
According to Alexander (2004), PD is evidently a progressive disorder which ultimately affects the nerve cells found within deeper regions of the human brain referred to as basal ganglia and substantia nigra. The nerve cells found in the substantia nigra will produce one of the neurotransmitters called dopamine which is believed to be accountable for the delay of the message which plans and controls the movement of the body. The nerve cells that produce dopamine found in the substantia nigra will gradually begin dying off in certain patients with PD. By the time where about 80 percent of dopamine is lost, the symptoms of DP including stiffness, tremor, balance problem and even slowness of movement, might be experienced. The movement of the body is mainly controlled by the complicated chain of decision that involves the inter-linked nerve cells groups referred to as the ganglia.
The message thus will come to the central regions of the brain referred to as striatum that operates with substantia nigra to send an impulse back and forth from an individual’s spinal cord to the brain. Both cerebellum and basal ganglia are primarily for making sure that the movement of the body is performed much smoothly and fluidly (De Lau & Breteler, 2006). The impulses are then passed from neuron to neuron and move from the brain regions to the spinal cord and ultimately to the regions of the muscles. In a situation where it happens that the dopamine receptor found in the striatum fails to get stimulated as required, the regions around the basal ganglia will automatically be over stimulated or under stimulated for instance. The subthalamic nucleus will become highly active and at the same time begin acting as brakes on the globus pallidus internal which ultimately results in the blackout of both the motion and rigidity.
Physiologically, research has shown that the symptoms and signs that are linked to are the final results massive loss of numbers of the neurotransmitters, typically dopamine (Smith & Kieval, 2000). The dopamine neurons’ degeneration has been shown to be common around the substantia nigra referred to as pars compacta. The increasing loss of the dopamine found at the pars compacta will in the process propel the drive of the excitatory around the basal ganglia which finally disrupt the normal functioning of the voluntary motor control which in the process causes the characteristics symptoms of the PD. The symptoms tend to get worse with time when more and more cells become infected by the illness are lost (Alexander, 2004).
According to Smith & Kieval, (2000), the dopamine actions are however opposed by a neurotransmitter referred to as acetylcholine. In a patient diagnosed with PD, the nerve cell which produces dopamine begins to die. The symptoms of both stiffness and tremor occur when nerve cells fires and at that time, there will be no adequate dopamine for the transmission of messages. The higher levels of glutamate will further emerge in PD when the body attempts compensating for the absence of dopamine. With severe PD, the depletion of the dopamine results in broader transformations around the basal ganglia pathway among them includes the changing role of serotonin, glutamate or even GABA.
Pathophysiology of the PD
The primary pathological features of PD include the death of cells found around the basal ganglia of the brain in addition to the Lewy bodies’ presence which is the amassing of protein alpha-synuclein in all the neurons that have remained. Alexander (2004) asserts that the increasing loss of neurons is argued to be experienced with the death of astrocyte in addition to the rise in the total numbers of microglia within the substantia nigra. There are about five critical paths in the brand that connects the rest of the brain regions with basal ganglia, and they include orbitofrontal circuits, motor, limbic, oculo-motor, in addition to the associative circuits where each name indicates the major projection regions of every circuit. Each of these areas is all influenced by PD, and further, their disturbance elucidates various symptoms of the illness because the circuits are in broader verities of function such as learning, movement, and attention.
De Lau & Breteler, (2006), highlight that the basal ganglia habitually put forth a continuous inhibitory effect on the broader variety of motor system thus preventing them from becoming active in suitable time. In a situation where a decision is made to execute a specific act, the inhibition is immediately condensed for the motor systems thus producing it for activation. Dopamine tends to play a critical role in aiding the production of inhibition; the hence higher intensity of dopamine function tends to promote the motor activities, while at the same time, lower levels of dopamine functions, that occurs in PD, requires the higher exertion of efforts for a particular movement. The overall net impact of dopamine exhaustion has been established to generate hypokinesia, which entails a decrease in the motor output.
There are speculations of various mechanisms by can results in the loss of the brain cells. One of the mechanisms is the anomalous buildup of protein alpha-synuclein bound to ubiquitin in the destroyed cells. Katzenschlager & Lees, (2002) posits that an insoluble protein thus will accumulate inside the neurons thus forming inclusion known as Lewy bodies which first appears in the pontine tegmentum, olfactory bulb, and medulla oblongata. An individual at this phase will become asymptomatic or even might develop specific early symptoms of non-motor. With the progression of the illness, Lewy bodies consequently develop around the substantia nigra, the regions of the midbrain in addition to the areas within the basal forebrain and around the neocortex. All these areas of the brain are the primary locations for the neuronal degeneration among the patients with PD, but Lewy bodies might not result in the death of cells (Alexander, 2004).
The Clinical Manifestations of PD
Cardinal characteristic of PD includes rigidity, tremor, rigidity and even bradykinesia. Postural unsteadiness does not often occur until later in the cause of the illness. The motor symptoms’ seriousness appears an independent forecaster of death among PD individuals. The tremor in PD apparently is a rest tremor which is mostly seen when gravity supports tremulous parts of the body. De Lau & Breteler (2006), point that the tremor often begins in the limbs of the fingers or hand. One might detect a back-and-forth forefinger’s and thumb’s rubbing referred to as the pill-rolling tremor. Essential tremor or multiple sclerosis is a situation where tremor takes place when the limb that has been affected is utilized. On PD patients might have a re-emergent tremor which manifests after few seconds with occurrence characteristic of other tremors in PD. De Lau & Breteler (2006), asserts that the tremor experienced during the initial periods of PD is discontinuous, and might not be evident to other people. Within a clinical setting, tremor is observed when the PD patient is relaxing with his hands placed on his laps.
The other symptom is the slowed movement also referred to as bradykinesia. Bradykinesia is the overall slowness of the patient’s movement, and it is considered the primary cause of the disability among PD patients and is common among all the patients. With time, PD might end up reducing the patient’s capability to move around and slow down the movements hence making the task more complicated and to consume a lot of time. The patient’s steps might also become shorter when walking or even find it challenging to get out of a chair (Katzenschlager & Lees, 2002).
The third symptom is the rigid muscles where muscle stiffness is experienced and mostly occurs in any part of the patient’s body a stiffened muscle might, in the end, limit an individual’s range of motions and thus causing much pain. Rigidity can be defined as the increased level of resistance to the passive movement around the joints and often occurs in about 90 percent of all individuals diagnosed with PD. As is the case in the symptoms’ of tremor and bradykinesia, rigidity also starts unilaterally. Eventually, rigidity progress to contralateral sides, and stay asymmetric all through the illness (Alexander, 2004).
The other clinical manifestation is the impaired posture and balance. Postural instability is one of the impairments of the centrally-mediated postural reflexes which often cause a feeling of imbalance in addition to the tendency to fall and a higher risk of injury. It usually appears later in the course of PD. The posture of the patient might become curved, or he might have balancing challenges due to PD (De Lau & Breteler, 2006). There is also the loss of automatic movements. Among Parkinson's patients, there is a higher possibility of a decreased ability to perform unconscious movements such as swinging of arms, blinking or even smiling. Speech changes are also a clinical manifestation where the patient will develop speech problems due to Parkinson's disease. At first, the patient will speak very softly, then fast, slur or even hesitate before speaking.
The Diagnostic Testing for PD
There is not the specific test used in diagnosis PD. A nervous system condition will, therefore, play a critical role in diagnosing the illness according to an individual’s medical history, reviewing the symptoms and finally, review the physical and neurological assessment. The physician will first assess for the PD with a carrying out a careful patient’s medical history in addition to the neurological evaluation. Alexander (2004), posits that an individual might be presented with levodopa where any consequential progression in the motor impairment will help to authenticate the diagnosis of the PD. Presence of the Lewy body at the brain on an autopsy is the ultimate evidence that an individual has PD (De Lau & Breteler, 2006). However, clinical course of the disease with time might tell that the condition is not PD demanding that there be a periodical review of the clinical presentation to confirm the diagnosis accuracy.
The physicians might thus order test including the blood tests to rule out other possible condition which could be causing the symptoms. A blood test will check for any abnormal thyroid hormone level or even liver damage. Imaging tests might also be conducted such as the MRI, PET and SPECT scans or even ultrasound of the brain to rule out other possible disorders. The imaging tests are not precisely helpful when it comes to diagnosing for PD, and besides, they are very expensive. Alexander (2004), notes that PET imaging will help to detect lower levels of dopamine in the patient’s brain.
In addition to the examination, the physician might go ahead to give the patient carbidopa-levodopa which is a Parkinson's disease medication, and it would be important that the dose is sufficient enough to show the benefit. Katzenschlager & Lees, (2002) asserts that significant improvement experienced with that medication will ultimately confirm the patient’s diagnosis of PD. Often, it takes a lot of time to diagnose PD; therefore the doctor might have to recommend a continuous follow-up appointment with the neurologists who is an expert in the movement disorder to assess the patient’s condition and symptoms over time and diagnose PD.
The Clinical Management and the Effect on the Pathophysiology Of PD
There is no specific treatment for PD; however, medications, physical therapy, and even surgery might provide significant relief and are believed to be to be highly efficient compared to the available treatments for other types of the neurological disorders like Parkinson plus syndromes, Alzheimer’s disease, and even motor neuron disease. The primary family of drugs that are often used in treating the motor symptoms includes levodopa, MAO-B inhibitors and even dopamine agonists (De Lau & Breteler, 2006). Usually, the stage of the illness together with age at disease onset has a significant role to play in determining the type of the group that is most suitable. Three distinct stage have been distinguished including; first, the initial phase where an individual diagnosed with PD has developed the specific disability that required the pharmacological treatment. The second phase which is related to the complication’s development related to the levodopa usage and the third stage that is primarily linked to symptoms unrelated to DP of the levodopa treatment might prevail (Katzenschlager & Lees, 2002).
At the last stage, the treatment is mainly aimed at an optimal trade-off between the side-effects of the treatment and the symptoms control. According to De Lau & Breteler (2006), the beginning of the levodopa treatment might be postponed through primarily making use of other medications like dopamine agonist and MAO-B inhibitor with the aim of delaying the complications’ onset as a result of the levodopa use. Conversely, levodopa has been considered to be one of the most effective forms of treatment for various PD symptoms; hence there would be no need to be postponed among the people whose quality of life is damaged by similar symptoms. Levodopa-related dyskinesia apparently correlates closely with the overall interval together with the relentlessness of PD than the levodopa treatment’s treatment. Therefore, it follows that delaying the therapy for PD patient might not offer much longer dyskinesia-free time than earlier usage (Alexander, 2004).
In the second phase, the primary intention is majorly to lessen the symptoms of PD while at the same time control the variation in the effects of the medications. Abrupt withdrawal from the medication or even instances of overuse should be managed efficiently (De Lau & Breteler, 2006). In a situation where oral medication is not adequate to control the symptoms, subcutaneous waking day apomorphine infusion, enteral dopa pumps and even deep brain stimulation might be suitable in this case. Finally, in the third stage, numerous challenging issues will be experienced, and this will ultimately require various treatments for the bladder dysfunction, psychiatric symptoms and orthostatic hypotension. Within the final stage of PD, there is the provision of the palliative care which is aimed at improving the overall quality of the patient’s life. De Lau & Breteler (2006), claims that patients diagnosed with PD are often reported to be challenging to manage as patients. Research has further shown that, the additional cognitive and the autonomic deficits, the level of complexity of the disease’s symptoms and the poor response to the majority of the PD treatment in addition to the rapid drop in the status apparently adds to problems in the management of these the people diagnosed with PD especially as the illnesses progress.
References
Alexander, G. E. (2004). Biology of Parkinson's disease: pathogenesis and pathophysiology of a multisystem neurodegenerative disorder. Dialogues in clinical neuroscience , 6 (3), 259.
De Lau, L. M., & Breteler, M. M. (2006). Epidemiology of Parkinson's disease. The Lancet Neurology , 5 (6), 525-535.
Katzenschlager, R., & Lees, A. J. (2002). Treatment of Parkinson's disease: levodopa as the first choice. Journal of neurology , 249 .
Smith, Y., & Kieval, J. Z. (2000). Anatomy of the dopamine system in the basal ganglia. Trends in neurosciences , 23 , S28-S33.
