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Explain the pathogenesis that leads to the structural and functional changes resulting from Mr George’s Parkinson’s disease.Explain how two of Mr George’s clinical manifestations are related to the structural and functional changes of his Parkinson’s disease.Select two drugs that have been used to treat Mr George’s Parkinson’s disease. Discuss the rationales for the administration of these drugs. Relate your discussion to the pathophysiological process



The first reason can be attributed to profession, as Mr. George is involved in teaching job and age factor, which is often accompanied with sitting or standing continuously, while delivering the education. These postures in regular terms may often induced oxidative stress over the body, which leads to alteration of physiological processes (Chenoweth, 2013). These is often linked with several signaling cascade and alteration in protein structure and function, which leads to triggering of undesired physiological characteristics. Another one is painful muscle cramps, which can be attributed to mitochondrial dys-functioning and hence lead to mis-folding of protein. It is noteworthy to mention that with the progressive ageing and increase in oxidative stress, the neuronal cells in brain use to degenerate and starts causing motor and non-motor complication associated with cognition, behavior and movement related disorders (Dissanayaka, 2011).

Notably the pathophysiology is related to degeneration of dopamine secretion cells in the substantia nigra of mid brain, which leads to deficiency of dopamine. This leads to alteration in the functioning of other functioning that are linked with the basal ganglia. These associated functioning is linked with motor, oculo-motor, limbic, associative, and orbitofrontal cascade of brain functioning. The tremor and rigidity in body parts is often accompanied with pain, which leads to difficulty in movement and corresponding slowness in movement. The difficulty in leaning, focusing, controlling the alteration in behavior and attention are linked with the complication. This leads to depletion in cholinergic and serotoninergic level in synaptic vesicles and cholinergic receptor. This leads to alteration in motor system, which often becomes active at inappropriate time. The inhibition, of the proliferated and inappropriate motor activities are in general uses to be inhibited by action of dopamine. Hence, the absence of dopamine lead to arise of the situation called Parkinson’s disease. The example of these proliferated and uncontrolled activities in Mr. George can be evidenced in the illustration of case study, such as monotonous speech, cramp in toes, stiffness in hand and legs, especially in the resting hours. Other than this, the changing of the facial expression and behavior alteration is also the example of the symptoms that are illustrated in the given case study is related to the clinical symptoms and consequences of the said pathophysiology of disorder. Other than this, the absence of timely detection and medication of the concerned cause also leads to proliferation of the problem, which is progression of the disease with time (Roeper, 2013).


First clinical manifestation is related to unilateral tremor, which reflects the death of more than 60 % dopamine producing neurons in the pars compacta region of substantia nigra of midbrain. These loss of neurons is furthermore reflected for deficiency of dopamine, which is requisite for the proper functioning of the central nervous system (Lukins, 2014). It should be noted that the sign and symptoms of the diseases are rare to come into picture, until more than 60 % of the dopamine producing cells are died in the brain parts. The attributes of degeneration of the brain parts are also linked with the age, which is also found in the give case. The age of Mr. George is 59+ and hence, it can be said that these extrapyramidal findings are fittings to the illustration in much accurate way (Dissanayaka, 2011). The next clinical manifestation is related to bradykinesia, which in other words is referred to as slowness in body movement and posture. Owing to the absence of role of biomolecule “dopamine” in the control of the motor functioning of brain, it leads to stiffness in body parts, which furthermore results in stiffness and slowness in body movement. This disorder is linked with symptoms of complication with nervous system. Notably, the appropriate means for the diagnosis of bradykinesia related symptoms is MRI scanning, to detect any tumor or dys-functioning of brain parts.


Amantadine, as such is an antiviral drug that is seldom used for the prophylaxis of influenza, but is also known to benefit the treatment of Parkinson’s disease serendipitously. The drug promotes the synthesis and release of dopamine by acting over the NMDA type of glutamate receptors. The said effect of stimulation of the synthesis is procured with the effect over striatal dopaminergic system. It is hence, it can be said that the agent is useful for supplementing the requirement of dopamine in brain (dopamine facilitator). Other than this, the advantage of usage is also linked with the suppression of motor fluctuations and abnormal movement cum coordination. It should be noted that the use is also accompanied with the side effects of dizziness and hallucination (Hollingworth, 2011).

Another drug is Entacapone, which is known as selective, potent and reversible COMT inhibitor. The agent is used as adjuvant to the supplement of levodopa in Parkinson patient. It should be noted that after the administration of levodopa, the peripheral decarboxylation of the agent is metabolized mainly by COMT, and produces 3-O methyldopa. Administration of Entacapone, thus inhibits the action on COMT over levodopa, and thereby the t1/2 of levodopa can be increased for action. In other words, it can be said that the present drug is capable of preserving the administered dopamine in the striatum and can thus supplement the peripheral effect in the brain (Korhonen, 2015).


Chenoweth, L., Sheriff, J., McAnally, L., & Tait, F. (2013). Impact of the Parkinson's disease medication protocol program on nurses' knowledge and management of Parkinson's disease medicines in acute and aged care settings. Nurse education today, 33(5), 458-464.


Dissanayaka, N. N., Sellbach, A., Silburn, P. A., O'Sullivan, J. D., Marsh, R., & Mellick, G. D. (2011). Factors associated with depression in Parkinson's disease. Journal of affective disorders, 132(1), 82-88.

Hollingworth, S. A., Rush, A., Hall, W. D., & Eadie, M. J. (2011). Utilization of anti‐Parkinson drugs in Australia: 1995–2009. Pharmacoepidemiology and drug safety, 20(5), 450-456.

Korhonen, P., Kuoppamäki, M., Prami, T., Hoti, F., Christopher, S., Ellmén, J., ... & Haukka, J. (2015). Entacapone and Prostate Cancer Risk in Patients With Parkinson's Disease. Movement Disorders.

Lukins, T. R., Tisch, S., & Jonker, B. (2014). The latest evidence on target selection in deep brain stimulation for Parkinson’s disease. Journal of Clinical Neuroscience, 21(1), 22-27.

Roeper, J. (2013). Dissecting the diversity of midbrain dopamine neurons. Trends in neurosciences, 36(6), 336-342.



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