Patient-Reported Outcome Severity and Emotional Salience Network Disruption in Multiple Sclerosis.


Journal

Brain imaging and behavior
ISSN: 1931-7565
Titre abrégé: Brain Imaging Behav
Pays: United States
ID NLM: 101300405

Informations de publication

Date de publication:
Jun 2022
Historique:
accepted: 02 12 2021
pubmed: 6 1 2022
medline: 18 5 2022
entrez: 5 1 2022
Statut: ppublish

Résumé

Overall burden of white matter damage is associated with increased self-report fatigue severity in people with multiple sclerosis. However, a paradoxically opposite association was reported for white matter damage to tracts in specific subnetworks including the amygdala, temporal pole, and insula. Based on neuroanatomical principles and other data from the literature, we hypothesized that these results might be indicative of a broader relationship between damage to these subnetworks and impaired recognition of negative emotional salience central to patient-reported outcomes. We examined whether damage in the same previously-identified subnetworks is also associated with lower self-report depressive symptoms, something which may be decreased in individuals with impaired recognition of negative emotional salience. Other patient characteristics were also explored. In a cohort of 137 people with multiple sclerosis, we measured location-specific network white matter tract damage in the proposed negative emotional salience network, along with self-report severity of depressive symptoms and cognitive problems, personality characteristics, objective cognitive performance, and physical disability. We applied regression analyses, accounting for lesion burden, to explore the relationship between damage in the proposed negative emotional salience network and these factors. We found disruption within the negative emotional salience network is associated with lower self-report depressive symptoms (β = -0.277, p = 0.036), cognitive complaints (r = -0.196, p = 0.024) and personality trait Neuroticism (r = -0.179, p = 0.042). In contrast, damage within this network was not significantly associated with objective cognitive processing speed, personality trait Openness, or physical disability. The identified network may be a generalizable network which corresponds to the recognition of negative emotional salience, but not to objective factors such as processing speed and physical disability. Damage to this network may paradoxically buffer against negative emotional perception of symptom severity, central to patient-reported outcomes.

Sections du résumé

BACKGROUND BACKGROUND
Overall burden of white matter damage is associated with increased self-report fatigue severity in people with multiple sclerosis. However, a paradoxically opposite association was reported for white matter damage to tracts in specific subnetworks including the amygdala, temporal pole, and insula. Based on neuroanatomical principles and other data from the literature, we hypothesized that these results might be indicative of a broader relationship between damage to these subnetworks and impaired recognition of negative emotional salience central to patient-reported outcomes.
OBJECTIVE OBJECTIVE
We examined whether damage in the same previously-identified subnetworks is also associated with lower self-report depressive symptoms, something which may be decreased in individuals with impaired recognition of negative emotional salience. Other patient characteristics were also explored.
METHODS METHODS
In a cohort of 137 people with multiple sclerosis, we measured location-specific network white matter tract damage in the proposed negative emotional salience network, along with self-report severity of depressive symptoms and cognitive problems, personality characteristics, objective cognitive performance, and physical disability. We applied regression analyses, accounting for lesion burden, to explore the relationship between damage in the proposed negative emotional salience network and these factors.
RESULTS RESULTS
We found disruption within the negative emotional salience network is associated with lower self-report depressive symptoms (β = -0.277, p = 0.036), cognitive complaints (r = -0.196, p = 0.024) and personality trait Neuroticism (r = -0.179, p = 0.042). In contrast, damage within this network was not significantly associated with objective cognitive processing speed, personality trait Openness, or physical disability.
CONCLUSION CONCLUSIONS
The identified network may be a generalizable network which corresponds to the recognition of negative emotional salience, but not to objective factors such as processing speed and physical disability. Damage to this network may paradoxically buffer against negative emotional perception of symptom severity, central to patient-reported outcomes.

Identifiants

pubmed: 34985619
doi: 10.1007/s11682-021-00614-5
pii: 10.1007/s11682-021-00614-5
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1252-1259

Informations de copyright

© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.

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Auteurs

Tom A Fuchs (TA)

Jacobs Multiple Sclerosis Center for Treatment and Research, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA. tomfuchs@buffalo.edu.
Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA. tomfuchs@buffalo.edu.

Caila B Vaughn (CB)

Jacobs Multiple Sclerosis Center for Treatment and Research, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.

Ralph H B Benedict (RHB)

Jacobs Multiple Sclerosis Center for Treatment and Research, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.

Bianca Weinstock-Guttman (B)

Jacobs Multiple Sclerosis Center for Treatment and Research, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.

Niels Bergsland (N)

Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.
IRCSS, Fondazione Don Carlo Gnocchi, Milan, Italy.

Dejan Jakimovski (D)

Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.

Deepa Ramasamy (D)

Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.

Robert Zivadinov (R)

Jacobs Multiple Sclerosis Center for Treatment and Research, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.
Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.
Center for Biomedical Imaging, Clinical Translational Science Institute, University at Buffalo, State University of New York (SUNY), Buffalo, NY, USA.

Michael G Dwyer (MG)

Jacobs Multiple Sclerosis Center for Treatment and Research, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.
Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York (SUNY), 100 High St, Buffalo, NY, 14203, USA.
Center for Biomedical Imaging, Clinical Translational Science Institute, University at Buffalo, State University of New York (SUNY), Buffalo, NY, USA.

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