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Running head Parkinsons Disease
Parkinsons Disease
Type your first name, middle initial, and last name
The State University of New York College at Old Westbury
In partial fulfillment for completion of PY3610 in the Department of Psychology.
Mentor/Advisor Wei Zhu, Ph.D.
Abstract
Parkinsons Disease
Introduction/Background
Parkinsons disease (PD) is generally characterized as a progressive neurodegenerative disorder. It was first founded by James Parkinson in 1817 therefore it is named after him. Clinically, Parkinsons disease is defined as the disorder related to the alteration in a movement of a person, but sometimes cognitive decline is also accompanied by motor problems. The dysfunctional movement and motor issues occur due to dopaminergic neurons selective degeneration in the Substania Nigra region of the brain. It is clinically characterized as bradykinesia which is the slow movement and resting has increased the chances of cure and survival even with this neuropsychological disorder. tremor. As the progression occurs in pathology, loss of movement starts happening and the development of postural instability. Motor dysfunction mostly occurs due to loss of olfaction, also known as hyposmia. Other symptoms in relation to non-motor dysfunction which develops with the progression of the disease, include hallucinations, dementia, depression, autonomic dysfunction, and sleep disturbances.
The Parkinsons disease has many different symptoms and ways of treatment and not everyone goes through the same condition or problem, therefore it varies from person to person. It took many years in getting rightly diagnosed by the neuropsychologists. The treatment and interventions were also poorly managed in the past, but now advancement in healthcare. It is a commonly occurring disease, such that everyone person in 10 goes through this disease in America. Parkinsons disease is generally described as an illness related to balance and posture. Therefore this paper will explore the neurological disorder of Parkinson disease in relation to other diseases and neuropsychological, neurobiological and neurochemical considerations.
2.0 Psychological Considerations
2.1 DSM-V Classification of the Biopsychological Disorder and its Associated Disorders
It is classified under the sub-section of major or mild neurocognitive disorders due to Parkinsons disease. It is included in criterion B and the deficits due to this disease are included in criterion C. the associated disorders of Parkinsons disease are as follows
Lewy bodies
Alzheimers disease
Vascular neurocognitive disorder
Another medical condition, i.e., delirium and neurocognitive disorders
Neuroleptic-induced parkinsonism
2.2 Psychological Symptoms
The only psychological symptoms related to this disease are depression, apathy, insomnia, hallucinations, delusions, anxiety, rapid eye movement sleep behavior disorder, personality changes, and excessive daytime sleepiness.
2.3 Behavioral Symptoms
It is a progressive degenerative disease therefore it affects the nerve cells in the deep parts of substantia nigra and basal ganglia in the brain. The symptoms include bradykinesia which is impaired dexterity, slowness of movement, drooling, decreased blinking, and expressionless face. Furthermore, resting tremor is characterized as involuntary shaking and rigidity and instability of posture (Trster, Jankovic, Tagliati, Peichel, Okun, 2017).
3.0 Neuropsychological Considerations
As Parkinsons disease is a neurocognitive degenerate disorder, the neuropsychological dysfunctions are associated with this disease. Apathy, along with the anxiety and depression is frequently occurring neuropsychological symptom in the patients of Parkinson disease, such that it is the higher in apathetic patients. Therefore, Pathophysiological indications suggest that the apathy in Parkinson disease is mainly due to dopaminergic denervation of the mesolimbic region, regardless of its well-known association is with the pathogenesis of anxiety and depression. Many studies indicated that the patients with apathy show a high level of serotonergic and dopaminergic degeneration in the putamen, bilateral caudate nuclei, pallidum and thalamus, ventral striatum, and a specific disruption in the bilateral dopaminergic region occur within the substantia Nigra and ventral tegmental area complex. Therefore, it reveals that serotoninergic degeneration is vital in neuropsychological considerations of Parkinsons disease (Ramdave, Dawson, Carter, Dissanayaka, 2019).
Furthermore, a study reported that in addition to apathy anxiety and depression are also commonly linked to Parkinsons disease. Due to the advanced neuroimaging, the area related to Parkinsons disease in the brain has been studied by the psychologist to be associated with the increase neural activity the regions of prefrontal cortex and limbic networks in the patients with depression. The functional imaging is inversely correlated with the density of dopaminergic activation in the putamen and caudate with the anxiety in the patients of Parkinsons disease.
4.0 Neurobiological, Neuroanatomical Neurochemical Considerations
Many studies and researches related to the considerations of neuropsychology in Parkinsons disease indicated towards the impairment in the cognitive task of the patient. The early onset of Parkinsons disease is detected through neuropsychological testing which can easily detect the dysfunction in executive tasks, attention, and memory. It is a systematic disease which represents various symptoms related to non-motor and motor functions. According to many studies the executive performance is dependent on the prefrontal cortex and structures related. The patients of Parkinsons disease have more activation in the cortex in relation to the lower deactivation this usually results in impaired motor functioning.
Moreover, other studies suggested that the deep brain stimulation surgery of a patient with Parkinsons disease exhibit the motor complications, intolerance to the treatment with drugs and unsatisfactory control. The age factor contributes to this matter, as patients with young age showed beneficial results. Other studies have shown that the patients of Parkinson disease are more prone towards dementia and they may develop dementia syndrome, and it is characterized by cholinergic and non-dopaminergic dysfunction of the cortex (Belaidi, Bush, 2016). This was possibly explored by the advancement in genetic research and neuroimaging. It revealed the substantial heterogeneity in the patients of Parkinson disease with the cognitive deficits range.
5.0 Neurochemical Considerations
The older patients with Parkinsons disease and major depressive disorder have altered levels of Hypothalamic-Pituitary-Adrenal, monoamine levels, axis dysfunctions, brain decreasing neurotrophic-derived factor, neuroinflammation and morphologic alterations in certain regions of the brain (Sampson, Debelius, Thron, Janssen, Shastri, Ilhan, Chesselet, 2016). According to the recent studies, the retina may be controlling functions of the deep brain and is prominently involved in the progression, etiology, and treatment of Parkinsons disease. Therefore, a certain study determined how dopamine, serotonin, and melatonin neurotransmitter systems in the retina, are individually involved in the control of the movement (Ascherio, Schwarzschild, 2016). Hence, the chemical pathology of Parkinsons disease relates to the degeneration of dopaminergic nigrostriatal track and it reduces the striatal dopamine. The distribution of dopamine is higher in the striatum and the depletion through reserpine also the dramatic effect of l-DOPA in reversing reserpine-induced tranquilization, resulted in dysfunctional ptosis and motor activity in rabbits and mice (Leo, Sarmento Silva, Santos, Ribeiro, Silva, 2015).
Consequently, the dysfunctional movement and motor issues occur due to dopaminergic neurons selective degeneration in the Substania Nigra region of the brain, and also other above-mentioned regions of the brain. The pathway of these neurons is towards the basal ganglia and is interconnected with other core structures of the brain. Various neuroscientists have utilized the functional and structural techniques for accessing brain functioning during the onset of Parkinsons disease. The advanced method or technique used is microdialysis, in which a small tube-like catheter is induced into the brain to explore the roles of glutamate and GABA during the tasks involved memory.
6.0 Discussion
There exist a wide range of aspects that contribute to the pervasive existence of the disease. As deliberated above, it is imperative to identify the symptoms and risk factors of Parkinsons disease thoroughly. Tremor, rigid muscles, speech changes, and the impaired posture and balance are the prominent symptoms which indicate that a person has established the disease. Primarily, the neurons in the brain slowly die or break down which initiates the disease. The loss of neurons further incites a chemical messenger called dopamine in the brain. Besides these facts, environmental triggers and genes are the prominent implications causes of Parkinsons disease. It is a contentious debate where the researchers are skeptical about the plausible changes that take place in mind.
A critical appraisal of the research highlights that the risk factors associated with the disease. Heredity plays an instrumental role in such circumstances. For instance, close proximity to the disease enhances the likelihood of the development of the disease. Men are prone to establishing the disease in comparison to women. The complications that surface after establishing the disease are detrimental and adverse. The emotional changes and depressed state of mind are the dominant impediments in the neurological system.
7.0 Conclusion
Consequently, this paper explored the neurological disorder of Parkinson disease, its symptoms etiology, and treatment in relation to other diseases and neuropsychological, neurobiological and neurochemical considerations. It is classified under the sub-section of major or mild neurocognitive disorders due to Parkinsons disease. The Parkinsons disease has many different symptoms and ways of treatment and not everyone goes through the same condition or problem, therefore it varies from person to person. As Parkinsons disease is a neurocognitive degenerate disorder, the neuropsychological dysfunctions are associated with this disease. Furthermore, a study reported that in addition to apathy anxiety and depression are also commonly linked to Parkinsons disease. The dysfunctional movement and motor issues in Parkinsons disease occur due to dopaminergic neurons selective degeneration in the Substania Nigra region of the brain, and also other above-mentioned regions of the brain. The advanced method or technique used such as microdialysis and many others are introduced in the patients to overcome the disease.
References
Ascherio, A., Schwarzschild, M. A. (2016). The epidemiology of Parkinsons disease risk factors and prevention. The Lancet Neurology, 15(12), 1257-1272.
Belaidi, A. A., Bush, A. I. (2016). Iron neurochemistry in Alzheimers disease and Parkinsons disease targets for therapeutics. Journal of Neurochemistry, 139, 179-197.
Leo, A. H., Sarmento Silva, A. J., Santos, J. R., Ribeiro, A. M., Silva, R. H. (2015). Molecular, Neurochemical, and Behavioral Hallmarks of Reserpine as a Model for Parkinsons Disease New Perspectives to a Long Standing Model. Brain Pathology, 25(4), 377-390.
Ramdave, S., Dawson, A., Carter, A., Dissanayaka, N. N. (2019). Unmasking neurobiological commonalities between addictive disorders and impulse control disorders in Parkinson s disease. Brain imaging and behavior, 1-14.
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hBCJOJQJaJphhBCJOJQJaJphhCJOJQJaJh4hCJOJQJaJ45589TUUUUUUUUUUUUUUUUUUUUUdgddgd0d0gd, J. W., Thron, T., Janssen, S., Shastri, G. G., Ilhan, Z. E., ... Chesselet, M. F. (2016). Gut microbiota regulates motor deficits and neuroinflammation in a model of Parkinsons disease. Cell, 167(6), 1469-1480.
Trster, A. I., Jankovic, J., Tagliati, M., Peichel, D., Okun, M. S. (2017). Neuropsychological outcomes from constant current deep brain stimulation for Parkinsons disease. Movement Disorders, 32(3), 433-440.
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