Differential Effects of Exercise on fMRI of the Midbrain Ascending Arousal Network Nuclei in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) and Gulf War Illness (GWI) in a Model of Postexertional Malaise (PEM).
GWI
Gulf War Illness
ME/CFS
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
PEM
arousal
autonomic
exercise
fMRI
midbrain
postexertional malaise
postural tachycardia
Journal
Brain sciences
ISSN: 2076-3425
Titre abrégé: Brain Sci
Pays: Switzerland
ID NLM: 101598646
Informations de publication
Date de publication:
05 Jan 2022
05 Jan 2022
Historique:
received:
22
11
2021
revised:
16
12
2021
accepted:
21
12
2021
entrez:
21
1
2022
pubmed:
22
1
2022
medline:
22
1
2022
Statut:
epublish
Résumé
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), Gulf War Illness (GWI) and control subjects underwent fMRI during difficult cognitive tests performed before and after submaximal exercise provocation (Washington 2020). Exercise caused increased activation in ME/CFS but decreased activation for GWI in the dorsal midbrain, left Rolandic operculum and right middle insula. Midbrain and isthmus nuclei participate in threat assessment, attention, cognition, mood, pain, sleep, and autonomic dysfunction. Activated midbrain nuclei were inferred by a re-analysis of data from 31 control, 36 ME/CFS and 78 GWI subjects using a seed region approach and the Harvard Ascending Arousal Network. Before exercise, control and GWI subjects showed greater activation during cognition than ME/CFS in the left pedunculotegmental nucleus. Post exercise, ME/CFS subjects showed greater activation than GWI ones for midline periaqueductal gray, dorsal and median raphe, and right midbrain reticular formation, parabrachial complex and locus coeruleus. The change between days (delta) was positive for ME/CFS but negative for GWI, indicating reciprocal patterns of activation. The controls had no changes. Exercise caused the opposite effects with increased activation in ME/CFS but decreased activation in GWI, indicating different pathophysiological responses to exertion and mechanisms of disease. Midbrain and isthmus nuclei contribute to postexertional malaise in ME/CFS and GWI.
Sections du résumé
BACKGROUND
BACKGROUND
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS), Gulf War Illness (GWI) and control subjects underwent fMRI during difficult cognitive tests performed before and after submaximal exercise provocation (Washington 2020). Exercise caused increased activation in ME/CFS but decreased activation for GWI in the dorsal midbrain, left Rolandic operculum and right middle insula. Midbrain and isthmus nuclei participate in threat assessment, attention, cognition, mood, pain, sleep, and autonomic dysfunction.
METHODS
METHODS
Activated midbrain nuclei were inferred by a re-analysis of data from 31 control, 36 ME/CFS and 78 GWI subjects using a seed region approach and the Harvard Ascending Arousal Network.
RESULTS
RESULTS
Before exercise, control and GWI subjects showed greater activation during cognition than ME/CFS in the left pedunculotegmental nucleus. Post exercise, ME/CFS subjects showed greater activation than GWI ones for midline periaqueductal gray, dorsal and median raphe, and right midbrain reticular formation, parabrachial complex and locus coeruleus. The change between days (delta) was positive for ME/CFS but negative for GWI, indicating reciprocal patterns of activation. The controls had no changes.
CONCLUSIONS
CONCLUSIONS
Exercise caused the opposite effects with increased activation in ME/CFS but decreased activation in GWI, indicating different pathophysiological responses to exertion and mechanisms of disease. Midbrain and isthmus nuclei contribute to postexertional malaise in ME/CFS and GWI.
Identifiants
pubmed: 35053821
pii: brainsci12010078
doi: 10.3390/brainsci12010078
pmc: PMC8774249
pii:
doi:
Types de publication
Journal Article
Langues
eng
Subventions
Organisme : United States Department of Defense
ID : W81XWH-15-1-0679
Organisme : United States Department of Defense
ID : W81-XWH-09-1-0526
Organisme : NINDS NIH HHS
ID : R21NS088138
Pays : United States
Organisme : NINDS NIH HHS
ID : RO1NS085131
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1TR000101
Pays : United States
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