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Abstract

Research Progress in Pathophysiological Mechanism of Dyskinesia in Parkinson's Disease

Author(s): Zhe Zhong, Min Xu, Lan Qing Yang, W. J. Chen, Huan Gao and Min Ye*
Department of Neurology, Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, Jiangsu 210019, China

Correspondence Address:
Min Ye, Department of Neurology, Affiliated BenQ Hospital of Nanjing Medical University, Nanjing, Jiangsu 210019, China, E-mail: yemin197001@sina.com


This study involves the research progress in pathophysiological mechanism of dyskinesia in Parkinson’s disease. Levodopa-induced dyskinesia is a complication characterized by involuntary movements in Parkinson’s patients after long-term treatment with levodopa. Dyskinesia is a kind of abnormal movement involving the face, neck, arm, leg and axial muscles. It often occurs on the serious side of the disease. It may be manifested as variety of phenomenologies, such as choreiform, dystonia, ballism, myoclonus and other forms of abnormal movements can manifest as well. At present, the research on the mechanisms of levodopa-induced dyskinesia is not yet fully understood. Nigrostriatal degeneration and levodopa administration are considered to be the basis of levodopa-induced dyskinesia. There appears to be variety mechanisms involved, such as abnormal dopaminergic transmission in presynaptic and postsynaptic membrane as well as non-dopaminergic systems. Nigrostriatal degeneration is considered to be the basis and premise of levodopa-induced dyskinesia. With the deepening of the research, non-dopaminergic systems such as glutamate, serotonin, adenosine, cholinergic and epinephrine have been proved to be involved in the occurrence of dyskinesia in animal models and clinical studies. This article is a more detailed review of the possible pathophysiological mechanisms of levodopa-induced dyskinesia, especially non-dopaminergic systems.

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