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Case Study

Case Analysis of Parkinsonism Disease

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Case Analysis of Parkinsonism Disease

Parkinson’s disease’s cause remains idiopathic, and it is among the common neurologic disorders that affect about one percent of people aged above 60 years. The disorder causes progressive disability, which can only be slowed through treatment. The pathophysiologic processes are due to the two neuropathologic findings, including the presence of Lewy bodies and the loss of pigmented dopaminergic neurons in the substantia nigra pars compacta.

In optimal brain functioning, there exists a balance between dopamine and acetylcholine neurotransmitters. When the disorder sets in, it is responsible for the progressive loss of pigmented dopaminergic neurons in the substantia nigra, and the Lewy bodies appear within the pigmented neurons. Over time, the disorder leads to the loss of approximately 60% to 80 % of the dopaminergic neurons, thus leading to motor disorders (Cook, shepherd, Boore & Dunleavy, 2019).  Disease progression leads to the destroying of the autonomic, limbic, and somatomotor systems components.

The basal ganglia, located in the midbrain, projects into the caudate nucleus, globus pallidus, and putamen collectively comprising the striatum. This part of the brain is critical in controlling posture and voluntary movements. Dopamine is the neurotransmitter produced by the cells in the nigra, and it is used by the nigrostriatal cells. Collectively the circuit completed by the motor cortex, basal ganglia, thalamus, and substantia nigra is called the nigrostriatal pathway. In this case, Parkinson’s disease leads to the loss of substantia nigra, causing dysfunctional stimuli to basal ganglia. Therefore, it leads to disruption of the circuit regulating output from the motor cortex.

In the case study, the disorder led to decreased levels of dopamine in the striatal and or degeneration of dopaminergic neurons in the nigrostriatal tract of the basal ganglia. The phenomenon led to abnormal neurotransmission, causing an imbalance of excitatory and inhibitory pathways of motor control; thus, causing excess cholinergic effects of cell excitation. Significant percentage loss of motor neurons due to the disease cause decreased dopamine levels manifests in the client (Prigent, Lionnet, Corbille & Derkinderen, 2017). Subsequently, the patient has the inability of motor neurons to generate and transmit signals. Therefore, from the case study, transmission inhibition caused the client to present with motor output symptoms, including fingers exhibiting a ‘pill-rolling movement, uneven gait. Besides, he shuffles when he walks, and his head/neck, hips, and knees are flexed forward, presents jerky or cogwheeling movement, resting arm and leg tremors, and stiffness.

Many factors have been studied and described to explain the possible impact of ethnicity and racial backgrounds on Parkinson’s disease. A recent review by Branson, Ferree, Hohler & Saint-Hilarie, 2016), there were highlighted reports of racial differences concerning many aspects of the disorder, ranging from knowledge of the disease in terms of diagnosis and management. Dietary habits that vary across ethnic groups have been shown to influence the disorder. For instance, decreased rates of manifesting Parkinson’s disease got associated with the Mediterranean diet (Erro, Brigo, Tamburin, et al., 2018; Alcalay, Gu, Mejia‐Santana, et al., 2012). Results a study carried out in Hong Kong revealed an increased rate of the disorder with the consumption of raw vegetables (Ho, Woo & Lee, 1989).

Additionally, differences in genetic factors across different racial groups have been suggested for consideration. According to Huang, Shu & Cai (2015), various genetic mutations influence differences across ethnic groups, including frequency and clinical manifestation of Parkinson’s disease. Barkhuizen, Anderson & Grobler describe that clinical expression of Parkinson’s disease varies regarding the underlying mutation (2016). Besides, glucocerebrosidase mutations have been associated with an increased non-motor symptoms burden, accompanied by high impaired cognitive function (Brockmann, Srulijes, Pflederer, et al., 2015). A study carried out in the United States indicated that individuals from minority backgrounds access the low quality of care and face many barriers to access health care (Lewey & Choudhry, 2014). Many pieces of the literature indicated small numbers regarding referrals for deep brain stimulation among African Americans compared to the whites (Branson, Ferree, Hohler & Saint-Hilarie, 2016). However, a survey on non-motor symptoms in Asian countries indicates a high prevalence of NMS among all ethnic groups (Sauerbier, A., Jitkritsadakul, O., Titova, et al., 2017).

 

 

 

 

 

 

 

 

 

 

 

 

References

Alcalay, R. N., Gu, Y., Mejia‐Santana, H., Cote, L., Marder, K. S., & Scarmeas, N. (2012). The association between Mediterranean diet adherence and Parkinson’s disease. Movement Disorders27(6), 771-774.

Barkhuizen, M., Anderson, D. G., & Grobler, A. F. (2016). Advances in GBA-associated Parkinson’s disease–Pathology, presentation, and therapies. Neurochemistry international93, 6-25.

Branson, C. O., Ferree, A., Hohler, A. D., & Saint-Hilarie, M. H. (2016). Racial disparities in Parkinson’s disease: a systematic review of the literature. Adv Parkinsons Dis5, 87-96.

Brockmann, K., Srulijes, K., Pflederer, S., Hauser, A. K., Schulte, C., Maetzler, W., … & Berg, D. (2015). GBA‐associated Parkinson’s disease: reduced survival and more rapid progression in a prospective longitudinal study. Movement Disorders30(3), 407-411.

Cook, N., Shepherd, A., Boore, J., & Dunleavy, S. (2019). Essentials of Pathophysiology for Nursing Practice. SAGE Publications Limited.

Erro, R., Brigo, F., Tamburin, S., Zamboni, M., Antonini, A., & Tinazzi, M. (2018). Nutritional habits, risk, and progression of Parkinson’s disease. Journal of neurology265(1), 12-23.

Ho, S. C., Woo, J., & Lee, C. M. (1989). Epidemiologic study of Parkinson’s disease in Hong Kong. Neurology39(10), 1314-1314.

Huang, T., Shu, Y., & Cai, Y. D. (2015). Genetic differences among ethnic groups. BMC genomics16(1), 1093.

Lewey, J., & Choudhry, N. K. (2014). The current state of ethnic and racial disparities in cardiovascular care: lessons from the past and opportunities for the future. Current cardiology reports16(10), 530.

Prigent, A., Lionnet, A., Corbille, A. G., & Derkinderen, P. (2017). Neuropathology and pathophysiology of Parkinson’s disease: Focus on α-synuclein. Presse medicale (Paris, France: 1983)46(2 Pt 1), 182-186.

Sauerbier, A., Jitkritsadakul, O., Titova, N., Klingelhoefer, L., Tsuboi, Y., Carr, H., … & Schrag, A. (2017). Non-motor symptoms assessed by Non-Motor Symptoms Questionnaire and Non-Motor Symptoms Scale in Parkinson’s disease in selected Asian populations. Neuroepidemiology49(1-2), 1-17.

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