Screen time in infancy is linked to changes in social-emotional development but the pathway underlying this association remains unknown. We aim to provide mechanistic insights into this association using brain network topology and to examine the potential role of parent–child reading in mitigating the effects of screen time.

We examined the association of screen time on brain network topology using linear regression analysis and tested if the network topology mediated the association between screen time and later socio-emotional competence. Lastly, we tested if parent–child reading time was a moderator of the link between screen time and brain network topology.

Infant screen time was significantly associated with the emotion processing-cognitive control network integration (p = 0.005). This network integration also significantly mediated the association between screen time and both measures of socio-emotional competence (BRIEF-2 Emotion Regulation Index, p = 0.04; SEARS total score, p = 0.04). Parent–child reading time significantly moderated the association between screen time and emotion processing-cognitive control network integration (β = −0.640, p = 0.005).

Our study identified emotion processing-cognitive control network integration as a plausible biological pathway linking screen time in infancy and later socio-emotional competence. We also provided novel evidence for the role of parent–child reading in moderating the association between screen time and topological brain restructuring in early childhood.

Inhibition capabilities have been shown to be a strong predictor of social and educational life outcomes (Mischel & Ebbesen, 1970; Shoda et al., 1990). Inhibition capabilities have an enormous impact on attention and impulsivity (Bari & Robbins, 2013). These two executive functions are associated with numerous psychiatric disorders but are not well understood in terms of white matter (WM) connectivity (Puiu et al., 2018). Novel techniques and statistical approaches in neuroimaging bring us closer to a biologically sustained model.

This research aims to: 1) identify WM connections associated with attention/impulsivity performance and 2) characterize the differences in WM microstructure associated with the variation of the performance.

157 children (GESTE cohort, 8-12 years, 27 Dx ADHD, 2 Dx ASD) with b=1500mm2/s, 2mm isotropic dMRI acquisitions were included. Tractography was performed with TractoFlow pipeline (Theaud et al., 2020). Dimensionality reduction of diffusion metrics yielded two components : microstructural complexity (DTI Metrics, AFD & NuFo) and axonal density (AFD_fixel) (Chamberland et al., 2019). Attention/impulsivity were evaluated with the CPT3. Multivariate linear regression was performed in python.

Lower microstructural complexity was associated with poorer attentional performance on regions of the parietal lobe to the occipital gyrus (P-O, p=0.044, R2=0.14, Figure 1.) and the Broadman’s area 8 to area 6 (SF8-SF6, p=0.002, R2=0.12, Figure 1.). Lower axonal density was associated with a less impulsive pattern on SF8-SF6 (p=0.001, R2=0.13, Figure 1.). Results remained significant when removing children with an ADHD or ASD diagnosis.

We identified underlying difference in WM microstructure that may be associated with the variation in attention/impulsivity performance in school-aged children.

No significant relationships.

The study was conducted to test the hypothesis that nitroglycerin (NTG) increases cerebral perfusion focally and globally in acute ischemic stroke patients, using serial perfusion-weighted imaging (PWI) magnetic resonance imaging measurements.

Thirty-five patients underwent PWI immediately before and 72 h after administration of a transdermal NTG patch or no treatment. Patients with baseline mean arterial pressure (MAP) > 100 mmHg (NTG group, n = 20) were treated with transdermal NTG (0.2 mg/h) for 72 h, without a nitrate-free interval. Patients with MAP ≤ 100 mmHg (untreated group, n = 15) were not treated. The primary outcome measure was absolute cerebral blood flow (CBF) in the hypoperfused region at 72 h.

The mean baseline absolute CBF in the hypoperfused region was similar in the NTG group (33.3 ± 10.2 ml/100 g/min) and untreated (32.7 ± 8.4 ml/100 g/min, p = 0.4) groups. The median (IQR) baseline infarct volume was 10.4 (2.5–49.3) ml in the NTG group and 32.6 (8.6–96.7) ml in the untreated group (p = 0.09). MAP change in the NTG group was 1.2 ± 12.6 and 8 ± 20.7 mmHg at 2 h and 72 h, respectively. Mean absolute CBF in the hypoperfused region at 72 h was similar in the NTG (29.9 ± 12 ml/100 g/min) and untreated groups (24.1 ± 10 ml/100 g/min, p = 0.8). The median infarct volume increased in untreated (11.8 (5.7–44.2) ml) than the NTG group (3.2 (0.5–16.5) ml; p = 0.033) on univariate analysis, however, there was no difference on regression analysis.

NTG was not associated with improvement in cerebral perfusion in acute ischemic stroke patients.

Leukoaraiosis, or white matter rarefaction, is a common imaging finding in aging and is presumed to reflect vascular disease. When severe in presentation, potential congenital or acquired etiologies are investigated, prompting referral for neuropsychological evaluation in addition to neuroimaging. T2-weighted imaging is the most common magnetic resonance imaging (MRI) approach to identifying white matter disease. However, more advanced diffusion MRI techniques may provide additional insight into mechanisms that influence the abnormal T2 signal, especially when clinical presentations are discrepant with imaging findings.

We present a case of a 74-year-old woman with severe leukoaraoisis. She was examined by a neurologist, neuropsychologist, and rheumatologist, and completed conventional (T1, T2-FLAIR) MRI, diffusion tensor imaging (DTI), and advanced single-shell, high b-value diffusion MRI (i.e., fiber ball imaging [FBI]).

The patient was found to have few neurological signs, no significant cognitive impairment, a negative workup for leukoencephalopathy, and a positive antibody for Sjogren’s disease for which her degree of leukoaraiosis would be highly atypical. Tractography results indicate intact axonal architecture that was better resolved using FBI rather than DTI.

This case illustrates exceptional cognitive resilience in the face of severe leukoaraiosis and the potential for advanced diffusion MRI to identify brain reserve.

Auditory verbal hallucinations (AVH) are a cardinal feature of schizophrenia, but they can also appear in otherwise healthy individuals. Imaging studies implicate language networks in the generation of AVH; however, it remains unclear if alterations reflect biologic substrates of AVH, irrespective of diagnostic status, age, or illness-related factors. We applied multimodal imaging to identify AVH-specific pathology, evidenced by overlapping gray or white matter deficits between schizophrenia patients and healthy voice-hearers.

Diffusion-weighted and T1-weighted magnetic resonance images were acquired in 35 schizophrenia patients with AVH (SCZ-AVH), 32 healthy voice-hearers (H-AVH), and 40 age- and sex-matched controls without AVH. White matter fractional anisotropy (FA) and gray matter thickness (GMT) were computed for each region comprising ICBM-DTI and Desikan–Killiany atlases, respectively. Regions were tested for significant alterations affecting both SCZ-AVH and H-AVH groups, relative to controls.

Compared with controls, the SCZ-AVH showed widespread FA and GMT reductions; but no significant differences emerged between H-AVH and control groups. While no overlapping pathology appeared in the overall study groups, younger (<40 years) H-AVH and SCZ-AVH subjects displayed overlapping FA deficits across four regions (p < 0.05): the genu and splenium of the corpus callosum, as well as the anterior limbs of the internal capsule. Analyzing these regions with free-water imaging ascribed overlapping FA abnormalities to tissue-specific anisotropy changes.

We identified white matter pathology associated with the presence of AVH, independent of diagnostic status. However, commonalities were constrained to younger and more homogenous groups, after reducing pathologic variance associated with advancing age and chronicity effects.

Research on psychobiological markers of Parkinson's disease (PD) remains a hot topic. Non-motor symptoms such as depression and REM sleep behavior disorder (RBD) each attribute to a particular neurodegenerative cluster in PD, and might enlighten the way for early prediction/detection of PD. The neuropathology of mood disturbances remains unclear. In fact, a few studies have investigated depression using diffusion magnetic resonance imaging (diffusion MRI).

Diffusion MRI of PD patients without comorbid RBD was used to assess whether microstructural abnormalities are detectable in the brain of 40 PD patients with depression compared to 19 patients without depression. Diffusion MRI connectometry was used to carry out group analysis between age- and gender-matched PD patients with and without depressive symptoms. Diffusion MRI connectometry is based on spin distribution function, which quantifies the density of diffusing water and is a sensitive and specific analytical method to psychological differences between groups.

A significant difference (FDR = 0.016129) was observed in the left and right uncinate fasciculi, left and right inferior longitudinal fasciculi, left and right fornices, left inferior fronto-occipital fasciculus, right corticospinal tract, genu of corpus callosum, and middle cerebellar peduncle.

These results suggest the prominent circuits involved in emotion recognition, particularly negative emotions, might be impaired in comorbid depressive symptoms in PD.

Volumetric atrophy and microstructural alterations in diffusion tensor imaging (DTI) measures of the hippocampus have been reported in people with Alzheimer's disease (AD) and mild cognitive impairment (MCI). However, no study to date has jointly investigated concomitant microstructural and volumetric changes of the hippocampus in dementia with Lewy bodies (DLB).

A total of 84 subjects (23 MCI, 17 DLB, 14 AD, and 30 healthy controls) were recruited for a multi-modal imaging (3T MRI and DTI) study that included neuropsychological evaluation. Freesurfer was used to segment the total hippocampus and delineate its subfields. The hippocampal segmentations were co-registered to the mean diffusivity (MD) and fractional anisotropy (FA) maps obtained from the DTI images.

Both AD and MCI groups showed significantly smaller hippocampal volumes compared to DLB and controls, predominantly in the CA1 and subiculum subfields. Compared to controls, hippocampal MD was elevated in AD, but not in MCI. DLB was characterized by both volumetric and microstructural preservation of the hippocampus. In MCI, higher hippocampal MD was associated with greater atrophy of the hippocampus and CA1 region. Hippocampal volume was a stronger predictor of memory scores compared to MD within the MCI group.

Through a multi-modal integration, we report novel evidence that the hippocampus in DLB is characterized by both macrostructural and microstructural preservation. Contrary to recent suggestions, our findings do not support the view that DTI measurements of the hippocampus are superior to volumetric changes in characterizing group differences, particularly between MCI and controls.