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Parkinson's Disease Assessment

Added on - 08 Dec 2020

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Research Methods Module
Table of ContentsINTRODUCTION...........................................................................................................................3BACKGROUND.............................................................................................................................4DISCUSSION OF POTENTIAL METHODOLOGIES.................................................................6TEST PROCEDURES...................................................................................................................11DISCUSSION OF ETHICS...........................................................................................................12REFERENCES..............................................................................................................................14
INTRODUCTIONFranciscus de le Böe (1614–1672) was the first person to describe tremors in his medicalwritings. Few other people who also documented certain aspects of this neurological conditionwere Francois Boissier de Sauvages de la Croix, William Shakespeare and Wilhelm vonHumboldt (Pahwa, 2003).A disease named Parkinson was named after Dr James Parkinson, a British physicianwho identified six subjects with a characteristic group of features (Pahwa, 2003). Based on allthe observations, he first described the clinical syndrome in 1817, with the title of: 'An essay onthe shaking palsy' (Szirmai, 2011). This idiopathic neurodegenerative disease mainly affectsmiddle or elder patients and is a little more common in men.To improve diagnostic accuracy, itis important to confirm the absence of atypical parkinsonism and the unilateral onset, which isvery typical in PD (Chien, 2016).Parkinson’s disease is one of the most common movement disorder that affects about 1%of adults older than 60 years (Samii, 2004). After the age of 50, risk of this disease increasessignificantly and increases further after 85 years (Adler&Ahlskog, 2000). Contrary Pahwa &et.al., states in their book that some researches have reported a drop in the prevalence after age79 i.e.”Lifetime risk for men 60 years of age is estimated at 4.6 % and for women 3.7 %”(Contrary Pahwa & et.al, 2003, pp. 39-40). Individual's with less than 40 years of age, the onsetof the disease is rare. At an early stage of Parkinson's disease, pathological lesions begin tooccur, but continues up to 3 decades until clinical symptoms appear (Adler&Ahlskog ,2000).Currently, diagnosis of this disease is still difficult because there is no biological marker,laboratory or instrumental test that can confirm its presence. The key indicators in diagnosis arethe four motor symptoms, which are: resting tremor, rigidity, bradykinesia and posturalinstability (Chien, 2016). Freezing and flexed posture are the most typical features ofparkinsonism. Presence of these symptoms helps in distinguishing PD from related parkinsoniandisorders. Secondary motor symptoms including but not limited to hypomimia, shuffling gait,festination, freezing, dystonia, non-motor symptoms as autonomic dysfunction, cognitive/neurobehavioral abnormalities, sensory abnormalities, paresthesias and pain (Jankovics, 2017).Ideally, every patient should have a baseline neuropsychological evaluation in order tofacilitate accurate detection and diagnosis, thus the evaluation of treatment effects(Pahwa ,2003). Parkinson's disease is more and more common, which means increasing
healthcare costs. The population is ageing and the estimated number of people with PD willdouble in the next three decades (Chien, 2016).BACKGROUNDThe exact cause of this disease is still unknown but according to the new nomenclature, itbelongs to the basal ganglion diseases (Szirmai, 2011) and during its progression the typicalasymmetric deficit persists (Adler & Ahlskog, 2000). Identification of substantial nigra asdopamine-producing cells occurred already in the 1960's and according to a discovery damage todopaminergic pathways leads to Parkinson's disease (Bentivoglio & Morelli, 2005). There areseveral theories about the cause of the disease, including the role of the immune system,apoptosis, neurotrophic factors, mitochondrial defects, genetic factors, central nervous systeminfections and the role of oxidative stress, moreover, the free radicals, which can lead to damageto the cellular lipid membrane, mitochondria and nucleic acids (Adler & Ahlskog, 2000).In 1957, dopamine was discovered as a putative neurotransmitter by Carlsson andcolleagues(Jankovic, 2017, pp.368). Ehringer and Hornykiewicz recognized that the dopaminelevel remarkably reduces in the stratum of patients with Parkinson disease and this discovery ledto the first trials of levodopa.Birkmayer andHornykiewicz studied the levodopa effectsonParkinson-akinesia in 1961(Jankovic, 2017).Levodopa is one of the most effective anti-Parkinson drug, in which the L-dopa iscombined with benserazide or carbidopa which prevents the formation of dopamine outside thenervous system, which further increases the effect on the nervous system. (Szirmai, 2011). Withthe use of Levodopa the life expectancy of patient increased, nevertheless, it remains lowercompared to the general population (Pahwa, 2003). It is important to mention the ON-OFFphenomenon which is the alternation of mobile ON and hypo-kinetic OFF phases. (Szirmai,2011).The onset of levodopa treatment is individual, depending on the Hoehn-Yahr stage. TheHoehn and Yahr Scale was published in 1967, to categorize the patients with Parkinson’s diseaseinto five stages of severity. It is commonly used and is rather simple and not to detailed,therefore the scale is not comprehensive and it focused only on the motor aspects of PD(Bhidayasiri & Tarsy, 2012). In Stages, I, II and III patients are only minimally disabled, whilepatients on Stage IV and V are severely disabled. (Hoehn & Yahr, 1967).
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