Capturing fatigue parameters: The impact of vagal processing in multiple sclerosis related cognitive fatigue.


Journal

Multiple sclerosis and related disorders
ISSN: 2211-0356
Titre abrégé: Mult Scler Relat Disord
Pays: Netherlands
ID NLM: 101580247

Informations de publication

Date de publication:
Jul 2019
Historique:
received: 21 01 2019
revised: 21 03 2019
accepted: 10 04 2019
pubmed: 22 4 2019
medline: 31 12 2019
entrez: 22 4 2019
Statut: ppublish

Résumé

Causes of fatigue in Multiple Sclerosis remain elusive. Recently, we developed a model linking cognitive fatigue to inflammatory processes based on a neuroinflammatory reflex-arc instantiated by the vagus nerve. The relation between experienced autonomic dysfunctions, based on vagal processing, and cognitive fatigue is well-known, but an examination of the association of objectively measured vagal activity and cognitive fatigue is missing. An attempt was made to collect behavioral and physiological evidence that can be associated with experienced autonomic dysfunctions and fatigue in Multiple Sclerosis patients. Behavioral performance (response bias) and autonomic functioning (Heart rate variability and Skin conductance level) during an acoustic vigilance task were investigated in 53 Multiple Sclerosis patients. We assessed trait fatigue (independent from task), and time-on-task related increase of fatigue. Regression analysis was used to predict the fatigue status with physiological and behavioral scores. Response bias, indicating a reduced responsiveness, and high and very low frequency components of Heart rate variability, indicating an increased parasympathetic activity, contribute to the regression of trait fatigue. Reduced Heart rate variability (SDNN) and increased parasympathetic activity (pNN50) remained in the regression model predicting time-on-task fatigue. Cognitive fatigue in MS is related to parasympathetic activity and reduced responsiveness, supporting our model representing fatigue as inflammatory processes in the brain. Standardized subjective and objective autonomous dysfunction measures might be considered as additional assessments in MS.

Sections du résumé

BACKGROUND BACKGROUND
Causes of fatigue in Multiple Sclerosis remain elusive. Recently, we developed a model linking cognitive fatigue to inflammatory processes based on a neuroinflammatory reflex-arc instantiated by the vagus nerve. The relation between experienced autonomic dysfunctions, based on vagal processing, and cognitive fatigue is well-known, but an examination of the association of objectively measured vagal activity and cognitive fatigue is missing. An attempt was made to collect behavioral and physiological evidence that can be associated with experienced autonomic dysfunctions and fatigue in Multiple Sclerosis patients.
METHODS METHODS
Behavioral performance (response bias) and autonomic functioning (Heart rate variability and Skin conductance level) during an acoustic vigilance task were investigated in 53 Multiple Sclerosis patients. We assessed trait fatigue (independent from task), and time-on-task related increase of fatigue. Regression analysis was used to predict the fatigue status with physiological and behavioral scores.
RESULTS RESULTS
Response bias, indicating a reduced responsiveness, and high and very low frequency components of Heart rate variability, indicating an increased parasympathetic activity, contribute to the regression of trait fatigue. Reduced Heart rate variability (SDNN) and increased parasympathetic activity (pNN50) remained in the regression model predicting time-on-task fatigue.
CONCLUSION CONCLUSIONS
Cognitive fatigue in MS is related to parasympathetic activity and reduced responsiveness, supporting our model representing fatigue as inflammatory processes in the brain. Standardized subjective and objective autonomous dysfunction measures might be considered as additional assessments in MS.

Identifiants

pubmed: 31005825
pii: S2211-0348(19)30173-7
doi: 10.1016/j.msard.2019.04.013
pii:
doi:

Types de publication

Clinical Trial Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

13-18

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

Auteurs

Carina Sander (C)

Institute of Psychology, Carl von Ossietzy University of Oldenburg, Department VI - Medicine and Health Sciences, Ammerländer Heerstr. 114-11826129, Oldenburg, Germany; Median Klinik Wilhelmshaven, Department of Neurology, Bremer Straße 2, 26382 Wilhelmshaven, Germany. Electronic address: carina.sander@uni-oldenburg.de.

Fenja Modes (F)

Institute of Psychology, Carl von Ossietzy University of Oldenburg, Department VI - Medicine and Health Sciences, Ammerländer Heerstr. 114-11826129, Oldenburg, Germany. Electronic address: fenja.modes@gmx.de.

Hans-Peter Schlake (HP)

Median Klinik Wilhelmshaven, Department of Neurology, Bremer Straße 2, 26382 Wilhelmshaven, Germany. Electronic address: HPSchlake@t-online.de.

Paul Eling (P)

Donders Institute for Brain, Cognition and Behavior, Radboud University Nijmegen, Montessorilaan 3, 6525 HR, Nijmegen, Netherlands. Electronic address: p.eling@donders.ru.nl.

Helmut Hildebrandt (H)

Institute of Psychology, Carl von Ossietzy University of Oldenburg, Department VI - Medicine and Health Sciences, Ammerländer Heerstr. 114-11826129, Oldenburg, Germany; Klinikum Bremen-Ost, Department of Neurology, Züricher Str. 40, 28325 Bremen, Germany. Electronic address: helmut.hildebrandt@uni-oldenburg.de.

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Classifications MeSH