100%(1)1 out of 1 people found this document helpful
This preview shows page 1 - 4 out of 14 pages.
Running head: PARKINSON’S DISEASE1Parkinson’s DiseaseDeena ZenderRasmussen CollegeAuthor NoteThis paper is being submitted on December 8, 2018, for Deena Zender’s NUR3205-06 Applied Pathophysiology course.
PARKINSON’S DISEASE2Parkinson’s DiseaseIn 1817, a British physician, James Parkinson, wrote about six different cases characterized by "involuntary tremulous motion, with lessened muscular power in parts not in action even when supported, with a propensity to bend their trunks forward from a walking to a running pace" (Ross & Singer, 2013). He called this disease shaking palsy, but in the modern world it’s known as Parkinson’s Disease (PD). PD is both a chronic and progressive disease; therefore, symptoms persist over a long period of time and get worse as the disease progresses (NINDS, 2018).PD is a motor system disorder and is accompanied by both systemic nonmotor and neurological symptoms. Degeneration of the basal ganglia involving the dopaminergic nigrostriatal pathway is the main distinguishing feature of the disease. Disorders of the nigrostriatal produce parkinsonism, a syndrome of abnormal movements. In PD, underactivity of the direct motor pathway causes unfacilitated movement, and overactivity of the indirect motor loop causes uninhibited movement, both of which are caused by a loss of dopamine neurons in the substantia nigra and a degeneration of the dopaminergic nigrostriatal pathway to the basal ganglia. This results in bradykinesia and rigidity due to the inhibition of the motor cortex, and the overactivity in the subthalamic nucleus influences the limbic system, affecting emotional signs and symptoms. In PD, dopamine loss is also found in the following areas of the brain: the brainstem, thalamus, and cortex. In cases of PD, half of individuals also have neuronal loss within the cerebral cortex. This loss causes cell dysfunction and death and includes the following: mitochondrial dysfunction, oxidative stress, altered protein handling, andinflammatory changes with autophagy and apoptosis. Some of the markers for neuronal degeneration include Lewy bodies, fibrillar intracellular eosinophilic inclusions, and high
PARKINSON’S DISEASE3concentrations of the alpha-synuclein, ubiquitin, tau protein, tuberculin, and other proteins found in the substantia nigra, locus ceruleus, and other areas of the brain. Degeneration of the locus ceruleus occurs in PD and may be associated with worsening of disease progression and the behavioral symptoms associated with PD. In the neurodegeneration of PD, molecular events associated with it may include mitochondrial dysfunction, oxidative stress, abnormal folding and accumulation of alpha-synuclein, abnormal phosphorylation, and dysfunction of the ubiquitin proteasome syndrome, which regulates the intracellular protein processing. Although all of this information is recognized, the pathogenesis of primary PD is still unknown (McCance & Huether, 2014).