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Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jul 7, 2016; 22(25): 5742-5752
Published online Jul 7, 2016. doi: 10.3748/wjg.v22.i25.5742
Gut dysfunction in Parkinson's disease
Adreesh Mukherjee, Atanu Biswas, Shyamal Kumar Das
Adreesh Mukherjee, Atanu Biswas, Shyamal Kumar Das, Department of Neurology, Bangur Institute of Neurosciences and Institute of Post Graduate Medical Education and Research, Kolkata, West Bengal 700025, India
Author contributions: All authors equally contributed to this paper with conception and design of the study, literature review and analysis, drafting and critical revision and editing, and final approval of the final version.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Shyamal Kumar Das, MD, DM, Professor, Head, Department of Neurology, Bangur Institute of Neurosciences and Institute of Post Graduate Medical Education and Research, 52/1A Sambhu Nath Pandit Street, Kolkata, West Bengal 700025, India. das_sk70@hotmail.com
Telephone: +91-33-22230003 Fax: +91-33-22236677
Received: March 27, 2016
Peer-review started: March 28, 2016
First decision: May 12, 2016
Revised: May 30, 2016
Accepted: June 15, 2016
Article in press: June 15, 2016
Published online: July 7, 2016
Processing time: 98 Days and 15.5 Hours
Core Tip

Core tip: Gut is involved in early Parkinson’s disease (PD) with extensive synuclein pathology, following a rostrocaudal gradient along the gastrointestinal system. It may act as the starting point of PD pathology with prion-like spread toward the central nervous system. The clinical manifestations include malnutrition, oral and dental disorders, sialorrhea, dysphagia, gastroparesis, constipation, and defecatory dysfunction. These are distressing for the patients and need to be managed properly by pharmacological or non-pharmacological measures. Gut dysfunction also leads to response fluctuations in PD and this may require alternative routes of administration or drug delivery systems for anti-PD medications.