The correspondence between morphometric MRI and metabolic profile in Rasmussen’s encephalitis

•The GM atrophy located in the insular and temporal cortices of the affected side.•Positive correlation was found in the brain region featuring MRI atrophy and FDG-PET.•GM atrophy was spatially correlated with dopaminergic and serotonergic mapping in RE. Volumetric magnetic resonance imaging (MRI) a...

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Published inNeuroImage clinical Vol. 33; p. 102918
Main Authors Tang, Chongyang, Ren, Peng, Ma, Kaiqiang, Li, Siyang, Wang, Xiongfei, Guan, Yuguang, Zhou, Jian, Li, Tianfu, Liang, Xia, Luan, Guoming
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.01.2022
Elsevier
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Online AccessGet full text
ISSN2213-1582
2213-1582
DOI10.1016/j.nicl.2021.102918

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Abstract •The GM atrophy located in the insular and temporal cortices of the affected side.•Positive correlation was found in the brain region featuring MRI atrophy and FDG-PET.•GM atrophy was spatially correlated with dopaminergic and serotonergic mapping in RE. Volumetric magnetic resonance imaging (MRI) atrophy is a hallmark of Rasmussen’s encephalitis (RE). Here, we aim to investigate voxel-wise gray matter (GM) atrophy in RE, and its associations with glucose hypometabolism and neurotransmitter distribution utilizing MRI and PET data. In this study, fifteen RE patients and fourteen MRI normal subjects were included in this study. Voxel-wise GM volume and glucose metabolic uptake were evaluated using structural MRI and FDG-PET images, respectively. Spatial Spearman’s correlation was performed between GM atrophy of RE with FDG uptake alterations, and neurotransmitter distributions provided in the JuSpace toolbox. Compared with the control group, RE patients displayed extensive GM volume loss not only in the ipsilateral hemisphere, but also in the frontal lobe, basal ganglia, and cerebellum in the contralateral hemisphere. Within the RE group, the insular and temporal cortices exhibited significantly more GM atrophy on the ipsilesional than the contralesional side. FDG-PET data revealed significant hypometabolism in areas surrounding the insular cortices in the ipsilesional hemisphere. RE-related GM volumetric atrophy was spatially correlated with hypomebolism in FDG uptake, and with spatial distribution of the dopaminergic and serotonergic neurotransmitter systems. The spatial concordance of morphological changes with metabolic abnormalities suggest FDG-PET offers potential value for RE diagnosis. The GM alterations associated with neurotransmitter distribution map could provide novel insight in understanding the neuropathological mechanisms and clinical feature of RE.
AbstractList Volumetric magnetic resonance imaging (MRI) atrophy is a hallmark of Rasmussen's encephalitis (RE). Here, we aim to investigate voxel-wise gray matter (GM) atrophy in RE, and its associations with glucose hypometabolism and neurotransmitter distribution utilizing MRI and PET data. In this study, fifteen RE patients and fourteen MRI normal subjects were included in this study. Voxel-wise GM volume and glucose metabolic uptake were evaluated using structural MRI and FDG-PET images, respectively. Spatial Spearman's correlation was performed between GM atrophy of RE with FDG uptake alterations, and neurotransmitter distributions provided in the JuSpace toolbox. Compared with the control group, RE patients displayed extensive GM volume loss not only in the ipsilateral hemisphere, but also in the frontal lobe, basal ganglia, and cerebellum in the contralateral hemisphere. Within the RE group, the insular and temporal cortices exhibited significantly more GM atrophy on the ipsilesional than the contralesional side. FDG-PET data revealed significant hypometabolism in areas surrounding the insular cortices in the ipsilesional hemisphere. RE-related GM volumetric atrophy was spatially correlated with hypomebolism in FDG uptake, and with spatial distribution of the dopaminergic and serotonergic neurotransmitter systems. The spatial concordance of morphological changes with metabolic abnormalities suggest FDG-PET offers potential value for RE diagnosis. The GM alterations associated with neurotransmitter distribution map could provide novel insight in understanding the neuropathological mechanisms and clinical feature of RE.Volumetric magnetic resonance imaging (MRI) atrophy is a hallmark of Rasmussen's encephalitis (RE). Here, we aim to investigate voxel-wise gray matter (GM) atrophy in RE, and its associations with glucose hypometabolism and neurotransmitter distribution utilizing MRI and PET data. In this study, fifteen RE patients and fourteen MRI normal subjects were included in this study. Voxel-wise GM volume and glucose metabolic uptake were evaluated using structural MRI and FDG-PET images, respectively. Spatial Spearman's correlation was performed between GM atrophy of RE with FDG uptake alterations, and neurotransmitter distributions provided in the JuSpace toolbox. Compared with the control group, RE patients displayed extensive GM volume loss not only in the ipsilateral hemisphere, but also in the frontal lobe, basal ganglia, and cerebellum in the contralateral hemisphere. Within the RE group, the insular and temporal cortices exhibited significantly more GM atrophy on the ipsilesional than the contralesional side. FDG-PET data revealed significant hypometabolism in areas surrounding the insular cortices in the ipsilesional hemisphere. RE-related GM volumetric atrophy was spatially correlated with hypomebolism in FDG uptake, and with spatial distribution of the dopaminergic and serotonergic neurotransmitter systems. The spatial concordance of morphological changes with metabolic abnormalities suggest FDG-PET offers potential value for RE diagnosis. The GM alterations associated with neurotransmitter distribution map could provide novel insight in understanding the neuropathological mechanisms and clinical feature of RE.
Volumetric magnetic resonance imaging (MRI) atrophy is a hallmark of Rasmussen’s encephalitis (RE). Here, we aim to investigate voxel-wise gray matter (GM) atrophy in RE, and its associations with glucose hypometabolism and neurotransmitter distribution utilizing MRI and PET data. In this study, fifteen RE patients and fourteen MRI normal subjects were included in this study. Voxel-wise GM volume and glucose metabolic uptake were evaluated using structural MRI and FDG-PET images, respectively. Spatial Spearman’s correlation was performed between GM atrophy of RE with FDG uptake alterations, and neurotransmitter distributions provided in the JuSpace toolbox. Compared with the control group, RE patients displayed extensive GM volume loss not only in the ipsilateral hemisphere, but also in the frontal lobe, basal ganglia, and cerebellum in the contralateral hemisphere. Within the RE group, the insular and temporal cortices exhibited significantly more GM atrophy on the ipsilesional than the contralesional side. FDG-PET data revealed significant hypometabolism in areas surrounding the insular cortices in the ipsilesional hemisphere. RE-related GM volumetric atrophy was spatially correlated with hypomebolism in FDG uptake, and with spatial distribution of the dopaminergic and serotonergic neurotransmitter systems. The spatial concordance of morphological changes with metabolic abnormalities suggest FDG-PET offers potential value for RE diagnosis. The GM alterations associated with neurotransmitter distribution map could provide novel insight in understanding the neuropathological mechanisms and clinical feature of RE.
• The GM atrophy located in the insular and temporal cortices of the affected side. • Positive correlation was found in the brain region featuring MRI atrophy and FDG-PET. • GM atrophy was spatially correlated with dopaminergic and serotonergic mapping in RE. Volumetric magnetic resonance imaging (MRI) atrophy is a hallmark of Rasmussen’s encephalitis (RE). Here, we aim to investigate voxel-wise gray matter (GM) atrophy in RE, and its associations with glucose hypometabolism and neurotransmitter distribution utilizing MRI and PET data. In this study, fifteen RE patients and fourteen MRI normal subjects were included in this study. Voxel-wise GM volume and glucose metabolic uptake were evaluated using structural MRI and FDG-PET images, respectively. Spatial Spearman’s correlation was performed between GM atrophy of RE with FDG uptake alterations, and neurotransmitter distributions provided in the JuSpace toolbox. Compared with the control group, RE patients displayed extensive GM volume loss not only in the ipsilateral hemisphere, but also in the frontal lobe, basal ganglia, and cerebellum in the contralateral hemisphere. Within the RE group, the insular and temporal cortices exhibited significantly more GM atrophy on the ipsilesional than the contralesional side. FDG-PET data revealed significant hypometabolism in areas surrounding the insular cortices in the ipsilesional hemisphere. RE-related GM volumetric atrophy was spatially correlated with hypomebolism in FDG uptake, and with spatial distribution of the dopaminergic and serotonergic neurotransmitter systems. The spatial concordance of morphological changes with metabolic abnormalities suggest FDG-PET offers potential value for RE diagnosis. The GM alterations associated with neurotransmitter distribution map could provide novel insight in understanding the neuropathological mechanisms and clinical feature of RE.
•The GM atrophy located in the insular and temporal cortices of the affected side.•Positive correlation was found in the brain region featuring MRI atrophy and FDG-PET.•GM atrophy was spatially correlated with dopaminergic and serotonergic mapping in RE. Volumetric magnetic resonance imaging (MRI) atrophy is a hallmark of Rasmussen’s encephalitis (RE). Here, we aim to investigate voxel-wise gray matter (GM) atrophy in RE, and its associations with glucose hypometabolism and neurotransmitter distribution utilizing MRI and PET data. In this study, fifteen RE patients and fourteen MRI normal subjects were included in this study. Voxel-wise GM volume and glucose metabolic uptake were evaluated using structural MRI and FDG-PET images, respectively. Spatial Spearman’s correlation was performed between GM atrophy of RE with FDG uptake alterations, and neurotransmitter distributions provided in the JuSpace toolbox. Compared with the control group, RE patients displayed extensive GM volume loss not only in the ipsilateral hemisphere, but also in the frontal lobe, basal ganglia, and cerebellum in the contralateral hemisphere. Within the RE group, the insular and temporal cortices exhibited significantly more GM atrophy on the ipsilesional than the contralesional side. FDG-PET data revealed significant hypometabolism in areas surrounding the insular cortices in the ipsilesional hemisphere. RE-related GM volumetric atrophy was spatially correlated with hypomebolism in FDG uptake, and with spatial distribution of the dopaminergic and serotonergic neurotransmitter systems. The spatial concordance of morphological changes with metabolic abnormalities suggest FDG-PET offers potential value for RE diagnosis. The GM alterations associated with neurotransmitter distribution map could provide novel insight in understanding the neuropathological mechanisms and clinical feature of RE.
Highlights•The GM atrophy located in the insular and temporal cortices of the affected side. •Positive correlation was found in the brain region featuring MRI atrophy and FDG-PET. •GM atrophy was spatially correlated with dopaminergic and serotonergic mapping in RE.
ArticleNumber 102918
Author Ren, Peng
Tang, Chongyang
Zhou, Jian
Liang, Xia
Wang, Xiongfei
Li, Siyang
Li, Tianfu
Ma, Kaiqiang
Luan, Guoming
Guan, Yuguang
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Keywords FDG-PET
TIV
VBM
MRI
GM
Voxel-based morphometry
SPECT
TPM
SPM
RE
Magnetic resonance imaging
Neurotransmitter
EPC
FLAIR
Rasmussen’s encephalitis
Positron emission tomography
ASDs
magnetic resonance imaging
anti-seizure drugs
total intracranial volume
fluid-attenuated inversion recovery
Fluorodeoxyglucose-positron emission tomography
single photon computed emission tomography
voxel-based morphometry
Statistic Parametric Mapping
gray matter
tissue probability map
epilepsia partialis continua
Rasmussen's encephalitis
Language English
License This is an open access article under the CC BY-NC-ND license.
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
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content type line 23
Chongyang Tang and Peng Ren contributed equally.
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SSID ssj0000800766
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Snippet •The GM atrophy located in the insular and temporal cortices of the affected side.•Positive correlation was found in the brain region featuring MRI atrophy and...
Highlights•The GM atrophy located in the insular and temporal cortices of the affected side. •Positive correlation was found in the brain region featuring MRI...
Volumetric magnetic resonance imaging (MRI) atrophy is a hallmark of Rasmussen's encephalitis (RE). Here, we aim to investigate voxel-wise gray matter (GM)...
• The GM atrophy located in the insular and temporal cortices of the affected side. • Positive correlation was found in the brain region featuring MRI atrophy...
Volumetric magnetic resonance imaging (MRI) atrophy is a hallmark of Rasmussen’s encephalitis (RE). Here, we aim to investigate voxel-wise gray matter (GM)...
SourceID doaj
pubmedcentral
proquest
pubmed
crossref
elsevier
SourceType Open Website
Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 102918
SubjectTerms Atrophy - pathology
Encephalitis - diagnostic imaging
Encephalitis - pathology
Gray Matter - diagnostic imaging
Gray Matter - pathology
Humans
Magnetic resonance imaging
Magnetic Resonance Imaging - methods
Metabolome
Neurotransmitter
Positron emission tomography
Radiology
Rasmussen’s encephalitis
Regular
Voxel-based morphometry
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Title The correspondence between morphometric MRI and metabolic profile in Rasmussen’s encephalitis
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https://www.clinicalkey.es/playcontent/1-s2.0-S2213158221003624
https://dx.doi.org/10.1016/j.nicl.2021.102918
https://www.ncbi.nlm.nih.gov/pubmed/34952352
https://www.proquest.com/docview/2614233224
https://pubmed.ncbi.nlm.nih.gov/PMC8713113
https://doaj.org/article/960cadd7898f47209047556dc7297989
Volume 33
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