Research-Based Interventions on Eating Disorders,
The Paraphilia and Neurocognitive Disorders
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Research-Based Interventions on Eating Disorders, the Paraphilia and Neurocognitive Disorders
Parkinson’s disease is a neurodegenerative disorder portrayed by the resting tremor presence, bradykinesia (extreme slowness in body movement and reflexes), postural instability, and rigidity (Dr. Hoehn, 1967). The level of progression and severity is determined by the ‘Hoehn and Yahr Scale’ established in 1967. The disease has five progression stages:
• First stage – The symptoms experienced may be minimal or unnoticed. The patient will experience tremors, slowness of movement in the arms or legs. Mild paralysis on one side of the face may be experienced resulting in non-uniform facial expression.
• Second stage – After several months or years, one may lose total facial expression ability, experience speech abnormalities and decreased blinking levels, onset of rigidity of muscles causing back or neck pain, and impaired body posture, but nevertheless the individual will be able to carry out normal daily tasks.
• Third stage – Characterized by the loss of balance and lack of the involuntary body responses when one is falling down. However, the patient is able to perform daily tasks such as eating, dressing independently.
• Fourth stage – Severity in the loss of balance; hence, there arises the need for a walking aid. The individual may be unable to perform all daily activities, thus needs assistance.
• Fifth stage – The individual is confined to a wheelchair and becomes fully dependent on others for chores performance . A significant loss of strength is observed, and the person becomes unable to rise from bed.
The onset of the disease is attributed to environmental or genetic factors. The genetic cause of Parkinson’s disease has been linked to the lack of dopamine in the brain tissues due to degradation of dopamine synthesizing cells in the substantia nigra. Dopamine is a neurotransmitter between the corpus striatum and substantia nigra. Decreased levels result in the loss of efficiency in the body movement due to impaired communication between the two areas (Goldman, 2014). The cause of cellular damage has been attributed to stress inflammation and dysfunctional cellular processes. The brain cells of majority of patients are found to have lewy bodies, abnormal clumps in the brain cells containing alpha ( synuclein protein (Patel et al., 2003). Members of families with a history of the disease are at a higher risk of developing the disease or hand down the defective genes to their offspring. Five genes identified in research connected to the disease include: SNCA (Synuclein, non A4 component of amyloid precursor), PARK 2 (Parkinson’s disease autosomal recessive, juvenile 2), PARK 7 (Parkinson’s disease autosomal recessive, early onset 7), PINK 1 (PTEN- induced putative kinase 1), and LRRK 2 (leucine-rich repeat kinase 2).
According to National Institute of Environment Health Science (NIEHS), environmental factors such as pesticides have been linked to causing the disease. Organochlorine insecticides such as DDT used to control mosquitoes and banned in the 1970s and 1980s contained residues associated with the disease. Due to its non-biodegradable chemical nature, it has persisted in the environment and nature for a long duration. Experimental trials on animal and human subjects proved that prolonged pesticide exposure increased the risk of developing the disease. Research conducted by NIEHS in 2013 found that people who
