scholarly journals White matter fascicles and cortical microstructure predict reading-related responses in human ventral temporal cortex

2020 ◽  
Author(s):  
Mareike Grotheer ◽  
Jason Yeatman ◽  
Kalanit Grill-Spector

AbstractReading-related responses in the lateral ventral temporal cortex (VTC) show a consistent spatial layout across individuals, which is puzzling, since reading skills are acquired during childhood. Here, we tested the hypothesis that white matter fascicles and gray matter microstructure predict the location of reading-related responses in lateral VTC. We obtained functional (fMRI), diffusion (dMRI), and quantitative (qMRI) magnetic resonance imaging data in 30 adults. fMRI was used to map reading-related responses by contrasting responses in a reading task with those in adding and color tasks; dMRI was used to identify the brain’s fascicles and to map their endpoints density in lateral VTC; qMRI was used to measure proton relaxation time (T1), which depends on cortical tissue microstructure. We fit linear models that predict reading-related responses in lateral VTC from endpoint density and T1 and used leave-one-subject-out cross-validation to assess prediction accuracy. Using a subset of our participants (N=10, feature selection set), we find that i) endpoint density of the arcuate fasciculus (AF), inferior longitudinal fasciculus (ILF), and vertical occipital fasciculus (VOF) are significant predictors of reading-related responses, and ii) cortical T1 of lateral VTC further improves the predictions of the fascicle model. Next, in the remaining 20 participants (validation set), we showed that a linear model that includes T1, AF, ILF and VOF significantly predicts i) the map of reading-related responses across lateral VTC and ii) the location of the visual word form area, a region critical for reading. Overall, our data-driven approach reveals that the AF, ILF, VOF and cortical microstructure have a consistent spatial relationship with an individual’s reading-related responses in lateral VTC.HighlightsThe ILF, AF, and VOF predict the spatial layout of reading-related responses in VTCGray matter microstructure improves the prediction of reading-related responsesFascicles and gray matter structure together predict the location of the VWFA

Neurology ◽  
2021 ◽  
pp. 10.1212/WNL.0000000000012869
Author(s):  
Raffaello Bonacchi ◽  
Alessandro Meani ◽  
Elisabetta Pagani ◽  
Olga Marchesi ◽  
Andrea Falini ◽  
...  

Objective:To investigate whether age at onset influences brain gray matter volume (GMV) and white matter (WM) microstructural abnormalities in adult multiple sclerosis (MS) patients, given its influence on clinical phenotype and disease course.Method:In this hypothesis-driven cross-sectional study, we enrolled 67 pediatric-onset MS (POMS) patients and 143 sex- and disease duration (DD)-matched randomly-selected adult-onset MS (AOMS) patients, together with 208 healthy controls. All subjects underwent neurological evaluation and 3T MRI acquisition. MRI variables were standardized based on healthy controls, to remove effects of age and sex. Associations with DD in POMS and AOMS patients were studied with linear models. Time to reach clinical and MRI milestones was assessed with product-limit approach.Results:At DD=1 year, GMV and WM fractional anisotropy (FA) were abnormal in AOMS but not in POMS patients. Significant interaction of age at onset (POMS vs AOMS) into the association with DD was found for GMV and WM FA. The crossing point of regression lines in POMS and AOMS patients was at 20 years of DD for GMV and 14 for WM FA. For POMS and AOMS patients, median DD was 29 and 19 years to reach Expanded Disability Status Scale=3 (p<0.001), 31 and 26 years to reach abnormal Paced Auditory Serial Addition Task-3 (p=0.01), 24 and 18 years to reach abnormal GMV (p=0.04), and 19 and 17 years to reach abnormal WM FA (p=0.36).Conclusions:Younger patients are initially resilient to MS-related damage. Then, compensatory mechanisms start failing with loss of WM integrity, followed by GM atrophy and finally disability.


1990 ◽  
Vol 73 (6) ◽  
pp. 864-870 ◽  
Author(s):  
Norihiko Tamaki ◽  
Takayuki Shirakuni ◽  
Kazumasa Ehara ◽  
Satoshi Matsumoto

✓ The magnetic resonance longitudinal relaxation time (T1) and transverse relaxation time (T2) of the water proton of the periventricular white and cortical gray matter were measured for 17 control patients and 21 patients with suspected normal-pressure hydrocephalus (NPH). Of the latter group, 14 showed good response to shunting (true-NPH group) and seven showed no response (false-NPH group). In the true-NPH group, both the T1 and the T2 of the periventricular white matter were significantly prolonged compared to the control values, and slowly shortened after cerebrospinal fluid (CSF) shunting. The true-NPH group showed significantly longer T1 and T2 of the white matter than did the false-NPH group. The T1 and T2 of the white matter were longer than those of the gray matter in this group, which was the reverse of the relationship observed in the control patients. In the white matter of the false-NPH group, there was a significant prolongation of T1 only; no difference was seen in the T2 compared to control values. There was no change in either T1 or T2 of this region after CSF shunting. The false-NPH group showed no significant difference in either T1 or T2 between the white and the gray matter. There was no difference in either T1 or T2 of the gray matter between the false-NPH and control groups or between preshunt and postshunt measurements in each patient group. It is suggested that a distinction between true- and false-NPH, which cannot be made from the radiographic appearance alone, may be possible from measurement of relaxation times. The mechanism of varied relaxation behavior between two entities may be explained by a difference in properties of the biological water and its environment.


2019 ◽  
Vol 116 (41) ◽  
pp. 20750-20759 ◽  
Author(s):  
Vaidehi S. Natu ◽  
Jesse Gomez ◽  
Michael Barnett ◽  
Brianna Jeska ◽  
Evgeniya Kirilina ◽  
...  

Human cortex appears to thin during childhood development. However, the underlying microstructural mechanisms are unknown. Using functional magnetic resonance imaging (fMRI), quantitative MRI (qMRI), and diffusion MRI (dMRI) in children and adults, we tested what quantitative changes occur to gray and white matter in ventral temporal cortex (VTC) from childhood to adulthood, and how these changes relate to cortical thinning. T1 relaxation time from qMRI and mean diffusivity (MD) from dMRI provide independent and complementary measurements of microstructural properties of gray and white matter tissue. In face- and character-selective regions in lateral VTC, T1 and MD decreased from age 5 to adulthood in mid and deep cortex, as well as in their adjacent white matter. T1 reduction also occurred longitudinally in children’s brain regions. T1 and MD decreases 1) were consistent with tissue growth related to myelination, which we verified with adult histological myelin stains, and 2) were correlated with apparent cortical thinning. In contrast, in place-selective cortex in medial VTC, we found no development of T1 or MD after age 5, and thickness was related to cortical morphology. These findings suggest that lateral VTC likely becomes more myelinated from childhood to adulthood, affecting the contrast of MR images and, in turn, the apparent gray–white boundary. These findings are important because they suggest that VTC does not thin during childhood but instead gets more myelinated. Our data have broad ramifications for understanding both typical and atypical brain development using advanced in vivo quantitative measurements and clinical conditions implicating myelin.


Neuron ◽  
2015 ◽  
Vol 85 (1) ◽  
pp. 216-227 ◽  
Author(s):  
Jesse Gomez ◽  
Franco Pestilli ◽  
Nathan Witthoft ◽  
Golijeh Golarai ◽  
Alina Liberman ◽  
...  

2018 ◽  
Author(s):  
Vaidehi S. Natu ◽  
Jesse Gomez ◽  
Michael Barnett ◽  
Brianna Jeska ◽  
Evgeniya Kirilina ◽  
...  

AbstractMicrostructural mechanisms underlying apparent cortical thinning during childhood development are unknown. Using functional, quantitative, and diffusion magnetic resonance imaging in children and adults, we tested if tissue growth (lower T1 relaxation time and mean diffusivity (MD)) or pruning (higher T1 and MD) underlies cortical thinning in ventral temporal cortex (VTC). After age 5, T1 and MD decreased in mid and deep cortex of functionally-defined regions in lateral VTC, and in their adjacent white matter. T1 and MD decreases were (i) consistent with tissue growth related to myelin proliferation, which we verified with adult postmortem histology and (ii) correlated with apparent cortical thinning. Thus, contrary to prevailing theories, cortical tissue does not thin during childhood, it becomes more myelinated, shifting the gray-white matter boundary deeper into cortex. As tissue growth is prominent in regions with protracted functional development, our data suggest an intriguing hypothesis that functional development and myelination are interlinked.


2013 ◽  
Vol 19 (11) ◽  
pp. 1485-1492 ◽  
Author(s):  
Mark Mühlau ◽  
Dorothea Buck ◽  
Annette Förschler ◽  
Christine C Boucard ◽  
Milan Arsic ◽  
...  

Background: In MS, the relationship between lesions within cerebral white matter (WM) and atrophy within deep gray matter (GM) is unclear. Objective: To investigate the spatial relationship between WM lesions and deep GM atrophy. Methods: We performed a cross-sectional structural magnetic resonance imaging (MRI) study (3 Tesla) in 249 patients with clinically-isolated syndrome or relapsing–remitting MS (Expanded Disability Status Scale score: median, 1.0; range, 0–4) and in 49 healthy controls. Preprocessing of T1-weighted and fluid-attenuated T2-weighted images resulted in normalized GM images and WM lesion probability maps. We performed two voxel-wise analyses: 1. We localized GM atrophy and confirmed that it is most pronounced within deep GM; 2. We searched for a spatial relationship between WM lesions and deep GM atrophy; to this end we analyzed WM lesion probability maps by voxel-wise multiple regression, including four variables derived from maxima of regional deep GM atrophy (caudate and pulvinar, each left and right). Results: Atrophy of each deep GM region was explained by ipsilateral WM lesion probability, in the area most densely connected to the respective deep GM region. Conclusion: We demonstrated that WM lesions and deep GM atrophy are spatially related. Our results are best compatible with the hypothesis that WM lesions contribute to deep GM atrophy through axonal pathology.


2018 ◽  
Vol 18 (10) ◽  
pp. 542 ◽  
Author(s):  
Vaidehi Natu ◽  
Jesse Gomez ◽  
Michael Barnett ◽  
Brianna Jeska ◽  
Zonglei Zhen ◽  
...  

2019 ◽  
Vol 30 (1) ◽  
pp. 326-338
Author(s):  
Xin Li ◽  
Jianan Xia ◽  
Chao Ma ◽  
Kewei Chen ◽  
Kai Xu ◽  
...  

Abstract Age is the major risk factor for Alzheimer’s disease (AD) and for mild cognitive impairment (MCI). However, there is limited evidence about MCI-specific aging-related simultaneous changes of the brain structure and their impact on cognition. We analyzed the brain imaging data from 269 subjects (97 MCI patients and 172 cognitively normal [CN] elderly) using voxel-based morphometry and tract-based spatial statistics procedures to explore the special structural pattern during aging. We found that the patients with MCI showed accelerated age-related reductions in gray matter volume in the left planum temporale, thalamus, and posterior cingulate gyrus. The similar age×group interaction effect was found in the fractional anisotropy of the bilateral parahippocampal cingulum white matter tract, which connects the temporal regions. Importantly, the age-related temporal gray matter and white matter alterations were more significantly related to performance in memory and attention tasks in MCI patients. The accelerated degeneration patterns in the brain structure provide evidence for different neural mechanisms underlying aging in MCI patients. Temporal structural degeneration may serve as a potential imaging marker for distinguishing the progression of the preclinical AD stage from normal aging.


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