A 67-year-old man presents to the HCP with chief complaint of tremors in his arms. He also has noticed some tremors in his leg as well. The patient is accompanied by his son, who says that his father has become “stiff” and it takes him much longer to perform simple tasks. The son also relates that his father needs help rising from his chair. Physical exam demonstrates tremors in the hands at rest and fingers exhibit “pill rolling” movement. The patient’s face is not mobile and exhibits a mask-like appearance. His gait is uneven, and he shuffles when he walks and his head/neck, hips, and knees are flexed forward. He exhibits jerky or cogwheeling movement. The patient states that he has episodes of extreme sweating and flushing not associated with activity. Laboratory data unremarkable and the HCP has diagnosed the patient with Parkinson’s Disease. Assignment (1- to 2-page case study analysis)
In your Case Study Analysis related to the scenario provided, explain the following:
Both the neurological and musculoskeletal pathophysiologic processes that would account for the patient presenting these symptoms.
Any racial/ethnic variables that may impact physiological functioning.
How these processes interact to affect the patient . Neurological and Musculoskeletal Disorders Essay Example
Week 8: Concepts of Neurological and Musculoskeletal Disorders – Part 2
Explain both the neurological and musculoskeletal pathophysiologic processes that would account for the patient presenting these symptoms. Explain any racial/ethnic variables that may impact physiological functioning. Explain how these processes interact to affect the patient.
The patient presents muscular rigidity, bradukinesia, resting tremor and postural instability, all symptoms that lead to the Parkinson’s disease diagnosis. These symptoms show a progressive loss of muscle control and mobility. Parkinson’s disease is associated with gradual loss of cells in the brain, particularly the substantia nigra area of the brain where the dopamine neurons in the nigor-striatal pathway are reported to degenerate. Dopamine is a chemical messenger that is produced in the brain. This messenger is responsible for transmitting signals between regions of the brain, and thereby coordinating activity. For instance, dopamine regulates muscle activity by connecting the corpus striatum to the substantia nigra. A deficiency of dopamine in the brain causes the striatum of the nerve cells to be out of control. This leaves the patient unable to control or direct musculoskeletal movements. This leads to the symptoms reported for Parkinson’s disease. As the disease progresses, other areas of the nervous system and brain degenerate (areas with neurons) resulting in the symptoms worsening with more profound movement disorder. Although the motor symptoms reported for Parkinson’s disease are attributed to striatal dopaminergic neurons being loss, the disease presents non-motor symptoms indicating that neural loss also occurs in nondopaminergic areas as well (Mancini, Nutt & Horak, 2019).
While the exact cause of cells in the substantia nigra being lost (so that dopamine production reduces) remains unknown, genetic and environmental factors have been identified as possible causes with the factors either acting in isolation or acting in combination. Certain genes have been associated with Parkinson’s disease. In fact, about 20% of all persons diagnosed with Parkinson’s disease have a close relative who has either been diagnosed with the disease or parkinsonian symptoms. In addition, the disease is reported at an early age among individuals with mutations in genes for glucocerebrosidase, DJ-1, LRRK2, PINK1, and parkin, among others. So far, there have been more than eight genetic mutations associated with the increased risk of an individual developing Parkinson’s disease (Müller, 2019).
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The National Institute of Neurological Disorders and Stroke (NINDS) and the National Human Genome Research Institute (NHGRI) pointed out alpha synculein gene (a gene on chromosome 4) that is liked to Parkinson’s disease developing among members of the same family. The changes/mutations in this gene are only thought to account for a small proportion of cases but is linked to a significant proportion of familial incidences of the disease with an onset before the age of 60 years. The alpha synculein gene is the main component of Lewy bodies that is found in the cells of all patients with the disease. Among persons in whom the gene is mutated, it is noted that an altered protein product is formed, and this protein accumulates in the cells while attracting other proteins. The aggregation of proteins form deposits that damage neurons (Haas, 2019).
In addition, the presence of free radicals has been associated with higher incidence of the disease. Free radicals are unstable molecules produced when normal chemical reactions occur in the body. The free radicals interact with other molecules in the body, resulting in neurons and other tissues being damaged. Besides that, aging is associated with the disease occurrence. Cell degeneration is a normal decline associated with aging. For older adults, aging causes a decline in the neurons that produce dopamine, resulting in dopamine loss so that the individual presents the symptoms of the disease. Furthermore, Parkinson’s disease is associated with environmental toxins. In this case, the environmental toxins get into the brain and cause damage to the brain cells. Some of the environmental toxins of note include herbicides and pesticides used in farming (Haas, 2019). Overall, any factor that causes damage to the brain cells or interrupts dopamine production can cause Parkinson’s disease.
Haas, R. H. (Eds.) (2019). Mitochondrial Dysfunction in Aging and Diseases of Aging. MDPI Books.
Mancini, M., Nutt, J. G., & Horak, F. B. (2019). Balance Dysfunction in Parkinson’s Disease: Basic Mechanisms to Clinical Management. Elsevier Science.
Müller, T. (Ed.) (2019). The Molecular and Cellular Basis for Parkinson’s Disease. MDPI Books. Neurological and Musculoskeletal Disorders Essay Example