Colonic transit, high-resolution anorectal manometry and MRI defecography study of constipation in Parkinson's disease.


Journal

Parkinsonism & related disorders
ISSN: 1873-5126
Titre abrégé: Parkinsonism Relat Disord
Pays: England
ID NLM: 9513583

Informations de publication

Date de publication:
09 2019
Historique:
received: 31 01 2019
revised: 27 08 2019
accepted: 27 08 2019
pubmed: 2 9 2019
medline: 5 8 2020
entrez: 2 9 2019
Statut: ppublish

Résumé

Despite clinical relevance and potential role on the disease pathogenesis, underlying mechanisms of constipation in Parkinson's disease (PD) remain poorly understood. A systematic assessment using complementary physiological investigations was performed to elucidate constipation pathophysiology in order to improve its symptomatic management. PD patients with constipation were evaluated with clinical questionnaires, colonic transit, high-resolution anorectal manometry and MRI defecography. Results were compared and correlated with clinical features. A total of 42 patients (69% male; age 68 ± 8 years; disease duration 10.5 ± 6.1 years) were included, of whom 33 (78.6%) had objective constipation defined by < 3 bowel movements per week or straining. Severity of constipation measured by self-administered questionnaires correlated with disease severity, burden of motor and non-motor symptoms but not with age, disease duration or Parkinson's medications. Colonic transit and anorectal function (high-resolution anorectal manometry and/or MRI defecography) was assessed in 15 patients. A combination of both delayed colonic transit and anorectal dysfunction was the pattern most commonly found (60% of patients) and overall anorectal dysfunction was more prevalent than isolated slow transit constipation. Physiological findings were heterogeneous including reduced colonic motility, rectal hyposensitivity, defecatory dyssynergia and poor motor rectal function. Subjective constipation in PD is poorly correlated with commonly used definition, assessment questionnaires and physiological results. Multiple complex overlapping pathophysiological mechanisms are responsible including slow transit and anorectal dysfunction. Complementary investigations to assess colonic transit and anorectal function are required in those with refractory symptoms for a systematic assessment and appropriate symptomatic management.

Identifiants

pubmed: 31473084
pii: S1353-8020(19)30372-4
doi: 10.1016/j.parkreldis.2019.08.016
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

195-201

Subventions

Organisme : Medical Research Council
ID : MR/L023784/1
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/L023784/2
Pays : United Kingdom

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

Auteurs

Eduardo De Pablo-Fernández (E)

Reta Lila Weston Institute of Neurological Studies, University College London Queen Square Institute of Neurology, 1 Wakefield Street, London, WC1N 1PJ, United Kingdom; Queen Square Brain Bank for Neurological Disorders, University College London Queen Square Institute of Neurology, 1 Wakefield Street, London, WC1N 1PJ, United Kingdom. Electronic address: eduardo.fernandez.13@ucl.ac.uk.

Valentina Passananti (V)

Gastrointestinal Physiology Unit, University College London Hospital, 235 Euston Road, London, NW1 2BU, United Kingdom. Electronic address: v.passananti@nhs.net.

Natalia Zárate-López (N)

Gastrointestinal Physiology Unit, University College London Hospital, 235 Euston Road, London, NW1 2BU, United Kingdom. Electronic address: n.zarate-lopez@nhs.net.

Anton Emmanuel (A)

Gastrointestinal Physiology Unit, University College London Hospital, 235 Euston Road, London, NW1 2BU, United Kingdom. Electronic address: a.emmanuel@ucl.ac.uk.

Thomas Warner (T)

Reta Lila Weston Institute of Neurological Studies, University College London Queen Square Institute of Neurology, 1 Wakefield Street, London, WC1N 1PJ, United Kingdom; Queen Square Brain Bank for Neurological Disorders, University College London Queen Square Institute of Neurology, 1 Wakefield Street, London, WC1N 1PJ, United Kingdom. Electronic address: t.warner@ucl.ac.uk.

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