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Structural and functional underpinnings of precentral abnormalities in amyotrophic lateral sclerosis
Author(s) -
Cheng Luqi,
Yuan Yumin,
Tang Xie,
Zhou Yuan,
Luo Chunxia,
Liu Daihong,
Zhang Yuanchao,
Zhang Jiuquan
Publication year - 2021
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/ene.14717
Subject(s) - precentral gyrus , amyotrophic lateral sclerosis , corpus callosum , neuroscience , white matter , fractional anisotropy , medicine , middle frontal gyrus , superior temporal gyrus , corticospinal tract , functional magnetic resonance imaging , superior frontal gyrus , magnetic resonance imaging , anatomy , diffusion mri , psychology , pathology , radiology , disease
Background and purpose Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by the loss of both upper and lower motor neurons. Studies using various magnetic resonance imaging (MRI) analytical approaches have consistently identified significant precentral abnormalities in ALS, whereas their structural and functional underpinnings remain poorly understood. Methods Using cortical thickness, fractional anisotropy (FA), and effective connectivity, we performed a multimodal MRI study to examine the structural and functional alterations associated with precentral abnormalities in patients with ALS ( n = 60) compared with healthy controls ( n = 60). Results Cortical thickness analysis revealed significant cortical thinning in the right precentral gyrus (PCG), superior frontal gyrus, and superior temporal gyrus in patients with ALS. Tractwise white matter microstructure analyses revealed decreased FA in the tracts connected to the PCG cluster in patients with ALS involving the right corticospinal tract and the middle posterior body of the corpus callosum. Additionally, the cortical thickness of the PCG cluster was found to be positively correlated with FA of the tracts connected to the PCG cluster, suggesting that these two structural features are tightly coupled. Using spectral dynamic causal modelling, effective connectivity analysis among the three regions with cortical thinning revealed decreased self‐inhibitory influence in the PCG cluster in patients with ALS, which might be an endophenotypic manifestation of an imbalance in inhibitory and excitatory neurotransmitters in this region. Conclusions The present data shed new light on the structural and functional underpinnings of precentral abnormalities in ALS.