Parkinson’s disease
Introduction
Parkinson’s disease is defined as a brain disorder that leads to shaking, stiffness, and difficulty with walking, balance, and coordination. Therefore, Parkinson’s symptoms gradually become worse over time. Therefore, as the progression of the disease continues, the patients eventually find it hard to walk and talk. They may also have mental and behavioural changes, sleep problems, depression, memory difficulties, and fatigue. This disease affects both women and men. However, the disease affects more women to men by about 50% of the score. A significant risk for Parkinson’s is age. In most people, the disease develops at the age of 60. Thus, about 5 to 10% of patients with the condition have “early-onset” symptoms in the disease. These symptoms begin at the age of 50. Parkinson’s early-onset forms of signs are, in most cases, inherited, some other arrangements linked to specific gene mutations.
History of Parkinson’s disease
Parkinson’s disease occurs when the nerve cells, or the neurons, in the brain area that controls movement become impaired, and the results are that the brain cells that control movement lose their function. These neurons regularly produce an essential brain chemical known as dopamine (Fujita, 2014). Therefore, when the neurons die, there is the production of less dopamine, thus causing the movement of Parkinson’s problems. Unfortunately, scientists do not know the cause of the less or dead dopamine production. Patients with Parkinson’s also lose their nerve endings that enable the creation of norepinephrine. Therefore, the chemical messenger of the sympathetic nervous system allows the control of the automatic functions in the body. Such include heart rate and blood pressure. The loss of norepinephrine causes the non-movement of Parkinson’s. The non-movement features include fatigue, irregular blood pressure, decreased movement of food in the digestive tract, and sudden drop in blood pressure, especially when a person stands up from a position of sitting (Fujita, 2014).
Lewy bodies develop in many patients with Parkinson’s disease, clumps that are unusual of protein alpha-synuclein. Scientists are doing their research to enable the understanding of both the standard and abnormal functions of alpha-synuclein; this relationship allows the genetic mutations as an impact on Parkinson’s disease, and Lewy body dementia. As stated above, Parkinson’s cases are, in most cases, hereditary. Only a few examples traced through specific genetic mutations, this situation has led many researchers to believe that Parkinson’s disease is a combination of genetic factors, and environmental factors such toxins exposure (Kong, 2014).
Symptoms of Parkinson’s disease
The four primary symptoms include; tremors, especially in the hands, arms, legs, jaws, and head. Stiffness of the limbs, and trucks, the movement appears to be slow, and impaired balance, and coordination, this may lead to falls. Other symptoms include depression and other emotional changes, swallowing difficulty, chewing difficulty, and speaking problems.
In most cases, medical tests that enable the detection of the disease make it challenging to diagnose the condition. Early symptoms of Parkinson’s disease are subtle, and the symptoms gradually occur. Friends and family members firstly notice the symptoms of this disease. Symptoms often begin on the patients, one side of the body, sometimes even on the limb of one side of the body. Then eventually, it affects both sides of the body. In some cases, the symptoms become more severe on one side rather than the other side of one’s body (Nalls, 2014).
Parkinson’s – Anatomy, Pathology, Prognosis, and Diagnosis
Parkinson’s disease considered predominantly basal ganglia.
Fig: 1 Parkinson’s disease
Shine, J. M., Halliday, G. M., Gilat, M., Matar, E., Bolitho, S. J., Carlos, M., … & Lewis, S. J. (2014). The role of the dysfunctional attentional control networks in visual misperceptions in Parkinson‘s disease. Human Brain Mapping, 35(5), 2206-2219.
The basal ganglia are a group of nuclei that is situated deep and centrally at the base of the forebrain. They have robust connections with a cerebral context and thalamus in addition to the other areas of the brain (Sarrafchi, 2016). Their vast system of communication enables the movement through a variety of functions, including automatic and voluntary motor control, procedural learning related to the routine behaviour, and moving services. The association with other cortical areas ensures a smooth orchestrated movement control and motor behaviour. The striatum is composed of both the Caudate and putamen and through a more massive nuclear complex of the basal of ganglia. The striatum received through the excitatory input from several areas of the cerebral cortex. The inhibitory and excitatory input from the dopaminergic cells of the substantia nigra pars compacta (SNc)
Pathology
The etiology of Parkinson’s is still unclear, especially with the hypotheses as to the diverse as peripheral versus central nervous system origin. The intrinsic cellular oscillator versus network oscillators, and basal ganglia-based on the pathophysiology versus the cerebellar-thalamic. Based on pathophysiology (Sarrafchi, 2014). However, using the pathological definition becomes a significant issue since it is not considered practical in this life. There two recognized neuropathological findings in the brains, especially in individuals with Parkinson’s. These include loss of pigmented dopaminergic neurons, and the presence of Lewy bodies, and Lewy neuritis (Schrag, 2015).
Fig: 2 the incidental Lewy bodies have been hypothesized to represent the pre-symptomatic phase of Parkinson
Source: Fujita, K. A., Ostaszewski, M., Matsuoka, Y., Ghosh, S., Glaab, E., Trefois, C., … & Diederich, N. (2014). Integrating pathways of Parkinson’s disease in a molecular interaction map. Molecular neurobiology, 49(1), 88-102.
- Localization of the significance of the cluster through the reduction of volume in Parkinson’s as compared to the people without the disease. Therefore, the significant group located in the Medulla oblongata/pons is superimposed as a red blob on the mean through the normalization of the anatomical scan from all the participants (Schrag, 2015)
Conclusion
Parkinson’s disease is therefore an illness that affects the brain system, affecting the movement of the patient’s body. It can come on so slowly that one may not notice the first symptoms. Parkinson’s disease is a progressive nervous system disorder that affects the movement of a patient. Early stages of the disease may show little or no experience, but with time symptoms worsen as the condition progresses. The disease does not have a cure, but with the right medications, the situation will improve. At times surgery might also be suggested to regulate certain regions which include, the brain, and this will lead to symptoms improvement.
References
Fujita, K. A., Ostaszewski, M., Matsuoka, Y., Ghosh, S., Glaab, E., Trefois, C., … & Diederich, N. (2014). Integrating pathways of Parkinson’s disease in a molecular interaction map. Molecular neurobiology, 49(1), 88-102.
Kong, S. M., Chan, B. K., Park, J. S., Hill, K. J., Aitken, J. B., Cottle, L., … & Cooper, A. A. (2014). Parkinson’s disease-linked human PARK9/ATP13A2 maintains zinc homeostasis and promotes α-Synuclein externalization via exosomes. Human molecular genetics, 23(11), 2816-2833.
Nalls, M. A., Pankratz, N., Lill, C. M., Do, C. B., Hernandez, D. G., Saad, M., … & Schulte, C. (2014). Large-scale meta-analysis of genome-wide association data identifies six new risk loci for Parkinson’s disease. Nature genetics, 46(9), 989.
Sarrafchi, A., Bahmani, M., Shirzad, H., & Rafieian-Kopaei, M. (2016). Oxidative stress and Parkinson’s disease: new hopes in treatment with herbal antioxidants. Current pharmaceutical design, 22(2), 238-246.
Schrag, A., Sauerbier, A., & Chaudhuri, K. R. (2015). New clinical trials for nonmotor manifestations of Parkinson’s disease. Movement Disorders, 30(11), 1490-1504.
Shine, J. M., Halliday, G. M., Gilat, M., Matar, E., Bolitho, S. J., Carlos, M., … & Lewis, S. J. (2014). The role of dysfunctional attentional control networks in visual misperceptions in Parkinson’s disease. Human Brain Mapping, 35(5), 2206-2219.