Abstract
Objectives:To determine (i) levodopa (L-Dopa) responsiveness on cortical functions, health related quality of life and fatigue severity (ii) relationship between cortical functions, health related quality of life and fatigue severity post L-Dopa treatment of patients with idiopathic Parkinson’s Disease (I-PD).Methods:Participants included 50 patients diagnosed with I-PD who were attending Civil and Bahawal Victoria Hospital, Bahawalpur, Pakistan during May 2016 to July 2017 and 50 healthy individuals (HI) took part in the study. Participants completed Cortical Function Assessment, Parkinson’s Disease Questionnaire and Fatigue Severity Scale. Patients were tested twice on these measures: pre and post- L-Dopa treatment.Results:Patients with I-PD showed cortical functioning deficits, deteriorated health related quality of life and experience of severe fatigue, in contrast with HI. There was significant improvement in cortical functioning and quality of life while reduction in fatigue severity was observed after three months of L-Dopa medication in I- PD patients. Higher cortical functioning deficits correlated with deteriorated health related quality of life and severe fatigue. Cortical functioning was a significant predictor of health related quality of life and fatigue severity.Conclusion:L-Dopa is an effective treatment for cortical dysfunctions, health related quality of life and fatigue in I-PD. Cortical functioning is a significant marker of quality of life and fatigue in patients with I-PD.
Highlights
Parkinson’s Disease (PD) is the second most common neurodegenerative disorder affecting 9 million people by 2030 in most populous nations1
Idiopathic Parkinson’s Disease (I-PD) is characterized by rigidity, tremor, and a kinesia due to several pathological mechanisms: activated microglia as evident in increased levels of [11C] (R)-PK11195 binding in cortical and subcortical regions compared to normal controls in Positron Emission Tomography[2], vulnerability of cortical areas and subcortical grays by formation of proteinaceous inclusion bodies beginning from dorsal motor nucleus in brain stem projecting upwards to mid brain, fore brain reaching cerebral cortex deteriorating limbic, autonomic and motor systems[3], continuous local presence of neurotoxin until death in the form of nigral Glutathione transferase activity and total glutathione deficiency as consequent of overutilization in response to oxidative stress[4], loss of corticocortical projection neurons, and striatal dopamine deficiency which
Post-treatment scores on Cortical Function Assessment12 (CFA) were inversely correlated with scores on FSS (r=-0.51, p
Summary
Parkinson’s Disease (PD) is the second most common neurodegenerative disorder affecting 9 million people by 2030 in most populous nations1. Idiopathic Parkinson’s Disease (I-PD) is characterized by rigidity, tremor, and a kinesia due to several pathological mechanisms: activated microglia as evident in increased levels of [11C] (R)-PK11195 binding in cortical and subcortical regions compared to normal controls in Positron Emission Tomography[2], vulnerability of cortical areas and subcortical grays by formation of proteinaceous inclusion bodies beginning from dorsal motor nucleus in brain stem projecting upwards to mid brain, fore brain reaching cerebral cortex deteriorating limbic, autonomic and motor systems[3], continuous local presence of neurotoxin until death in the form of nigral Glutathione transferase activity and total glutathione deficiency as consequent of overutilization in response to oxidative stress[4], loss of corticocortical projection neurons, and striatal dopamine deficiency which
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