TY - JOUR
T1 - Vulnerability of Thalamic Nuclei at CSF Interface During the Entire Course of Multiple Sclerosis
AU - for OFSEP investigators
AU - Koubiyr, Ismail
AU - Yamamoto, Takayuki
AU - Blyau, Simon
AU - Kamroui, Reda A.
AU - Mansencal, Boris
AU - Planche, Vincent
AU - Petit, Laurent
AU - Saranathan, Manojkumar
AU - Casey, Romain
AU - Ruet, Aurélie
AU - Brochet, Bruno
AU - Manjón, José V.
AU - Dousset, Vincent
AU - Coupé, Pierrick
AU - Tourdias, Thomas
N1 - Publisher Copyright:
© 2024 American Academy of Neurology.
PY - 2024/4/18
Y1 - 2024/4/18
N2 - Background and Objectives Thalamic atrophy can be used as a proxy for neurodegeneration in multiple sclerosis (MS). Some data point toward thalamic nuclei that could be affected more than others. However, the dynamic of their changes during MS evolution and the mechanisms driving their differential alterations are still uncertain. Methods We paired a large cohort of 1,123 patients with MS with the same number of healthy controls, all scanned with conventional 3D-T1 MRI. To highlight the main atrophic regions at the thalamic nuclei level, we validated a segmentation strategy consisting of deep learning–based synthesis of sequences, which were used for automatic multiatlas segmentation. Then, through a lifespan–based approach, we could model the dynamics of the 4 main thalamic nuclei groups. Results All analyses converged toward a higher rate of atrophy for the posterior and medial groups compared with the anterior and lateral groups. We also demonstrated that focal MS white matter lesions were associated with atrophy of groups of nuclei when specifically located within the associated thalamocortical projections. The volumes of the most affected posterior group, but also of the anterior group, were better associated with clinical disability than the volume of the whole thalamus. Discussion These findings point toward the thalamic nuclei adjacent to the third ventricle as more susceptible to neurodegeneration during the entire course of MS through potentiation of disconnection effects by regional factors. Because this information can be obtained even from standard T1-weighted MRI, this paves the way toward such an approach for future monitoring of patients with MS.
AB - Background and Objectives Thalamic atrophy can be used as a proxy for neurodegeneration in multiple sclerosis (MS). Some data point toward thalamic nuclei that could be affected more than others. However, the dynamic of their changes during MS evolution and the mechanisms driving their differential alterations are still uncertain. Methods We paired a large cohort of 1,123 patients with MS with the same number of healthy controls, all scanned with conventional 3D-T1 MRI. To highlight the main atrophic regions at the thalamic nuclei level, we validated a segmentation strategy consisting of deep learning–based synthesis of sequences, which were used for automatic multiatlas segmentation. Then, through a lifespan–based approach, we could model the dynamics of the 4 main thalamic nuclei groups. Results All analyses converged toward a higher rate of atrophy for the posterior and medial groups compared with the anterior and lateral groups. We also demonstrated that focal MS white matter lesions were associated with atrophy of groups of nuclei when specifically located within the associated thalamocortical projections. The volumes of the most affected posterior group, but also of the anterior group, were better associated with clinical disability than the volume of the whole thalamus. Discussion These findings point toward the thalamic nuclei adjacent to the third ventricle as more susceptible to neurodegeneration during the entire course of MS through potentiation of disconnection effects by regional factors. Because this information can be obtained even from standard T1-weighted MRI, this paves the way toward such an approach for future monitoring of patients with MS.
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U2 - 10.1212/NXI.0000000000200222
DO - 10.1212/NXI.0000000000200222
M3 - Article
C2 - 38635941
AN - SCOPUS:85191104020
SN - 2332-7812
VL - 11
JO - Neurology: Neuroimmunology and NeuroInflammation
JF - Neurology: Neuroimmunology and NeuroInflammation
IS - 3
M1 - e200222
ER -