Neural responses to psychological stress predict the future course of quality of life and neuropsychiatric symptoms in multiple sclerosis patients
ECTRIMS Online Library. Meyer-Arndt L. 09/13/19; 278512; P1310
Lil Meyer-Arndt
Lil Meyer-Arndt
Contributions
Abstract

Abstract: P1310

Type: Poster Sessions

Abstract Category: Pathology and pathogenesis of MS - Neuropsychology

L. Meyer-Arndt1, S. Hetzer2, S. Asseyer1, J. Bellmann-Strobl1,3, M. Scheel1, A.U. Brandt1, J.-D. Haynes1,2,4, F. Paul1,5,6, S.M. Gold7,8,9, M. Weygandt1

1NeuroCure Clinical Research Center, 2Berlin Center for Advanced Neuroimaging, Charite - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 3Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, 4Bernstein Center for Computational Neuroscience, 5Experimental and Clinical Research Center, 6Department of Neurology, Charite - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, 7Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, 8Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, 9Department of Psychosomatic Medicine, Charite - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany

Prospective clinical studies support an association between psychological stress and disability in multiple sclerosis (MS). Consistently, we showed in a recent cross-sectional functional MRI study ('neurological severity study' in the following) that brain activity during a psychological stress task is linked to clinical disability and grey matter (GM) atrophy in persons with MS (PwMS). Consequently, we tested here whether this activity also predicts the future course of neuropsychiatric symptoms (i.e., fatigue, depressive symptoms, social exclusion, and cognition) and quality of life (QoL) assessed with the Hamburg Quality of Life Questionnaire in Multiple Sclerosis (HAQUAMS).
In the neurological severity study, we used a mental arithmetic task comprising performance-dependent task speed adaptation and feedback to induce stress. We computed voxel-wise perfusion differences assessing fast (i.e. differences for the stress minus a pre-stress resting period) and slow stress effects (post- minus pre-stress rest). Here, we related these parameters taken from 27 (23 relapsing-remitting, 4 secondary progressive) PwMS participating in the neurological severity study to their variations in HAQUAMS scores occurring between this baseline study visit ('T0') and a follow-up visit ('T1').
The average time-lapse between T0 and T1 was 851 (SD = 176) days. Across all GM coordinates, primarily slow stress responses in a parahippocampal coordinate were associated with longitudinal QoL worsening (t = 7.74; pFamily-Wise Error [FWE] corrected = 0.0014). Constraining our analysis to limbic regions, especially slow hippocampal stress responses were linked to worsening of depressive symptoms (t = 4.96; pFWE = 0.0198).
We show that stress-induced brain activity predicts the course of QoL and neuropsychiatric symptoms in PwMS. The positive link between activity in memory-related limbic areas and worsening of QoL and depressive symptoms suggests that stronger recall of percepts coupled to the stress experience in the past could be a source of longitudinal symptom exacerbation which possibly constitutes a modifiable disease factor.
Disclosure:
Lil Meyer-Arndt: Nothing to disclose.
Stefan Hetzer: Nothing to dislose.
Susanna Asseyer: Received travel grant fees from celgene, unrelated to this project.
Judith Bellmann-Strobl: Received travel grants and speaking fees from Bayer Healthcare, Biogen Idec, Merck Serono, Sanofi Genzyme, Teva Pharmaceuticals, and Novartis.
Michael Scheel: Holds a patent for manufacturing of phantoms for computed tomography imaging with 3D printing technology and received research support from Federal Ministry of Economics and Technology.
Alexander U. Brandt: Served on the scientific advisory board for Biogen; received travel funding and/or speaker honoraria from Novartis and Biogen; has patents pending from method and system for optic nerve head shape quantification, perceptive visual computing based postural control analysis, multiple sclerosis biomarker, and perceptive sleep motion analysis; has consulted for Nexus and Motognosis; received research support from Novartis Pharma, Biogen Idec, BMWi, BMBF, and Guthy Jackson Charitable Foundation; go to Neurology.org/nn for full disclosure forms.
John-Dylan Haynes: Nothing to disclose.
Friedemann Paul: Serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate editor for Neurology® Neuroimmunology &Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA.
Stefan M. Gold: Received honoraria from Celgene, Almirall, and Mylan'.
Martin Weygandt: Nothing to disclose.

Abstract: P1310

Type: Poster Sessions

Abstract Category: Pathology and pathogenesis of MS - Neuropsychology

L. Meyer-Arndt1, S. Hetzer2, S. Asseyer1, J. Bellmann-Strobl1,3, M. Scheel1, A.U. Brandt1, J.-D. Haynes1,2,4, F. Paul1,5,6, S.M. Gold7,8,9, M. Weygandt1

1NeuroCure Clinical Research Center, 2Berlin Center for Advanced Neuroimaging, Charite - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, 3Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine and Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt Universität zu Berlin, and Berlin Institute of Health, 4Bernstein Center for Computational Neuroscience, 5Experimental and Clinical Research Center, 6Department of Neurology, Charite - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, 7Institute of Neuroimmunology and Multiple Sclerosis (INIMS), Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, 8Department of Psychiatry and Psychotherapy, Campus Benjamin Franklin, 9Department of Psychosomatic Medicine, Charite - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany

Prospective clinical studies support an association between psychological stress and disability in multiple sclerosis (MS). Consistently, we showed in a recent cross-sectional functional MRI study ('neurological severity study' in the following) that brain activity during a psychological stress task is linked to clinical disability and grey matter (GM) atrophy in persons with MS (PwMS). Consequently, we tested here whether this activity also predicts the future course of neuropsychiatric symptoms (i.e., fatigue, depressive symptoms, social exclusion, and cognition) and quality of life (QoL) assessed with the Hamburg Quality of Life Questionnaire in Multiple Sclerosis (HAQUAMS).
In the neurological severity study, we used a mental arithmetic task comprising performance-dependent task speed adaptation and feedback to induce stress. We computed voxel-wise perfusion differences assessing fast (i.e. differences for the stress minus a pre-stress resting period) and slow stress effects (post- minus pre-stress rest). Here, we related these parameters taken from 27 (23 relapsing-remitting, 4 secondary progressive) PwMS participating in the neurological severity study to their variations in HAQUAMS scores occurring between this baseline study visit ('T0') and a follow-up visit ('T1').
The average time-lapse between T0 and T1 was 851 (SD = 176) days. Across all GM coordinates, primarily slow stress responses in a parahippocampal coordinate were associated with longitudinal QoL worsening (t = 7.74; pFamily-Wise Error [FWE] corrected = 0.0014). Constraining our analysis to limbic regions, especially slow hippocampal stress responses were linked to worsening of depressive symptoms (t = 4.96; pFWE = 0.0198).
We show that stress-induced brain activity predicts the course of QoL and neuropsychiatric symptoms in PwMS. The positive link between activity in memory-related limbic areas and worsening of QoL and depressive symptoms suggests that stronger recall of percepts coupled to the stress experience in the past could be a source of longitudinal symptom exacerbation which possibly constitutes a modifiable disease factor.
Disclosure:
Lil Meyer-Arndt: Nothing to disclose.
Stefan Hetzer: Nothing to dislose.
Susanna Asseyer: Received travel grant fees from celgene, unrelated to this project.
Judith Bellmann-Strobl: Received travel grants and speaking fees from Bayer Healthcare, Biogen Idec, Merck Serono, Sanofi Genzyme, Teva Pharmaceuticals, and Novartis.
Michael Scheel: Holds a patent for manufacturing of phantoms for computed tomography imaging with 3D printing technology and received research support from Federal Ministry of Economics and Technology.
Alexander U. Brandt: Served on the scientific advisory board for Biogen; received travel funding and/or speaker honoraria from Novartis and Biogen; has patents pending from method and system for optic nerve head shape quantification, perceptive visual computing based postural control analysis, multiple sclerosis biomarker, and perceptive sleep motion analysis; has consulted for Nexus and Motognosis; received research support from Novartis Pharma, Biogen Idec, BMWi, BMBF, and Guthy Jackson Charitable Foundation; go to Neurology.org/nn for full disclosure forms.
John-Dylan Haynes: Nothing to disclose.
Friedemann Paul: Serves on the scientific advisory board for Novartis; received speaker honoraria and travel funding from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Merck Serono, Alexion, Chugai, MedImmune, and Shire; is an academic editor for PLoS ONE; is an associate editor for Neurology® Neuroimmunology &Neuroinflammation; consulted for SanofiGenzyme, Biogen Idec, MedImmune, Shire, and Alexion; received research support from Bayer, Novartis, Biogen Idec, Teva, Sanofi-Aventis/Genzyme, Alexion, Merck Serono, German Research Council, Werth Stiftung of the City of Cologne, German Ministry of Education and Research, Arthur Arnstein Stiftung Berlin, EU FP7 Framework Program, Arthur Arnstein Foundation Berlin, Guthy Jackson Charitable Foundation, and National Multiple Sclerosis of the USA.
Stefan M. Gold: Received honoraria from Celgene, Almirall, and Mylan'.
Martin Weygandt: Nothing to disclose.

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