Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome

We recruited 43 Chronic Fatigue Syndrome (CFS) subjects who met Fukuda criteria and 27 healthy controls and performed 3T MRI T1 and T2 weighted spin-echo (T1wSE and T2wSE) scans. T1wSE signal follows T1 relaxation rate (1/T1 relaxation time) and responds to myelin and iron (ferritin) concentrations....

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Main Authors: Leighton R. Barnden, Zack Y. Shan, Donald R. Staines, Sonya Marshall-Gradisnik, Kevin Finegan, Timothy Ireland, Sandeep Bhuta
Format: Article
Language:English
Published: Elsevier 2018-01-01
Series:NeuroImage: Clinical
Online Access:http://www.sciencedirect.com/science/article/pii/S2213158218302237
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spelling doaj-60dba74b2c994b8080d0d8a46337d62c2020-11-25T02:16:43ZengElsevierNeuroImage: Clinical2213-15822018-01-0120102109Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndromeLeighton R. Barnden0Zack Y. Shan1Donald R. Staines2Sonya Marshall-Gradisnik3Kevin Finegan4Timothy Ireland5Sandeep Bhuta6National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute Queensland, Griffith University, Southport, QLD 4222, Australia; Corresponding author at: National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute Queensland, Griffith University, Southport, QLD 4222, Australia.National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute Queensland, Griffith University, Southport, QLD 4222, AustraliaNational Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute Queensland, Griffith University, Southport, QLD 4222, AustraliaNational Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute Queensland, Griffith University, Southport, QLD 4222, AustraliaMedical Imaging Department, Gold Coast University Hospital, Parklands, QLD 4215, AustraliaMedical Imaging Department, Gold Coast University Hospital, Parklands, QLD 4215, AustraliaMedical Imaging Department, Gold Coast University Hospital, Parklands, QLD 4215, AustraliaWe recruited 43 Chronic Fatigue Syndrome (CFS) subjects who met Fukuda criteria and 27 healthy controls and performed 3T MRI T1 and T2 weighted spin-echo (T1wSE and T2wSE) scans. T1wSE signal follows T1 relaxation rate (1/T1 relaxation time) and responds to myelin and iron (ferritin) concentrations. We performed MRI signal level group comparisons with SPM12. Spatial normalization after segmentation was performed using T2wSE scans and applied to the coregistered T1wSE scans. After global signal-level normalization of individual scans, the T1wSE group comparison detected decreased signal-levels in CFS in a brainstem region (cluster-based inference controlled for family wise error rate, PFWE= 0.002), and increased signal-levels in large bilateral clusters in sensorimotor cortex white matter (cluster PFWE < 0.0001). Moreover, the brainstem T1wSE values were negatively correlated with the sensorimotor values for both CFS (R2 = 0.31, P = 0.00007) and healthy controls (R2 = 0.34, P = 0.0009), and the regressions were co-linear. This relationship, previously unreported in either healthy controls or CFS, in view of known thalamic projection-fibre plasticity, suggests brainstem conduction deficits in CFS may stimulate the upregulation of myelin in the sensorimotor cortex to maintain brainstem – sensorimotor connectivity. VBM did not find group differences in regional grey matter or white matter volumes. We argued that increased T1wSE observed in sensorimotor WM in CFS indicates increased myelination which is a regulatory response to deficits in the brainstem although the causality cannot be tested in this study. Altered brainstem myelin may have broad consequences for cerebral function and should be a focus of future research. Keywords: Chronic Fatigue Syndrome, Brainstem, Motor, Sensorimotor, T1wSE, Myelin, Upregulationhttp://www.sciencedirect.com/science/article/pii/S2213158218302237
collection DOAJ
language English
format Article
sources DOAJ
author Leighton R. Barnden
Zack Y. Shan
Donald R. Staines
Sonya Marshall-Gradisnik
Kevin Finegan
Timothy Ireland
Sandeep Bhuta
spellingShingle Leighton R. Barnden
Zack Y. Shan
Donald R. Staines
Sonya Marshall-Gradisnik
Kevin Finegan
Timothy Ireland
Sandeep Bhuta
Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome
NeuroImage: Clinical
author_facet Leighton R. Barnden
Zack Y. Shan
Donald R. Staines
Sonya Marshall-Gradisnik
Kevin Finegan
Timothy Ireland
Sandeep Bhuta
author_sort Leighton R. Barnden
title Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome
title_short Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome
title_full Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome
title_fullStr Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome
title_full_unstemmed Hyperintense sensorimotor T1 spin echo MRI is associated with brainstem abnormality in chronic fatigue syndrome
title_sort hyperintense sensorimotor t1 spin echo mri is associated with brainstem abnormality in chronic fatigue syndrome
publisher Elsevier
series NeuroImage: Clinical
issn 2213-1582
publishDate 2018-01-01
description We recruited 43 Chronic Fatigue Syndrome (CFS) subjects who met Fukuda criteria and 27 healthy controls and performed 3T MRI T1 and T2 weighted spin-echo (T1wSE and T2wSE) scans. T1wSE signal follows T1 relaxation rate (1/T1 relaxation time) and responds to myelin and iron (ferritin) concentrations. We performed MRI signal level group comparisons with SPM12. Spatial normalization after segmentation was performed using T2wSE scans and applied to the coregistered T1wSE scans. After global signal-level normalization of individual scans, the T1wSE group comparison detected decreased signal-levels in CFS in a brainstem region (cluster-based inference controlled for family wise error rate, PFWE= 0.002), and increased signal-levels in large bilateral clusters in sensorimotor cortex white matter (cluster PFWE < 0.0001). Moreover, the brainstem T1wSE values were negatively correlated with the sensorimotor values for both CFS (R2 = 0.31, P = 0.00007) and healthy controls (R2 = 0.34, P = 0.0009), and the regressions were co-linear. This relationship, previously unreported in either healthy controls or CFS, in view of known thalamic projection-fibre plasticity, suggests brainstem conduction deficits in CFS may stimulate the upregulation of myelin in the sensorimotor cortex to maintain brainstem – sensorimotor connectivity. VBM did not find group differences in regional grey matter or white matter volumes. We argued that increased T1wSE observed in sensorimotor WM in CFS indicates increased myelination which is a regulatory response to deficits in the brainstem although the causality cannot be tested in this study. Altered brainstem myelin may have broad consequences for cerebral function and should be a focus of future research. Keywords: Chronic Fatigue Syndrome, Brainstem, Motor, Sensorimotor, T1wSE, Myelin, Upregulation
url http://www.sciencedirect.com/science/article/pii/S2213158218302237
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