Haldguerrero3647

Children who have been diagnosed with autism spectrum disorder (ASD) often show a marked deficit in measures of social cognition. In autistic adults, measures of social cognition have been shown to relate to differences in brain synchronization (as measured by fMRI) when individuals are processing naturalistic stimuli, such as movies. However, whether children who differ in their degree of autistic traits, with or without a diagnosis of ASD, differ in their neural responses to movies has not yet been investigated. In the current study, neural synchrony, measured using fMRI, was examined in three groups of children aged 7 to 12, who differed with respect to scores on a measure of autistic traits associated with social impairment and whether or not they had been diagnosed with ASD. While watching the movie 'Despicable Me', those diagnosed with ASD had significantly less neural synchrony in areas that have been previously shown to be associated with social cognition (e.g. Dorsomorphin areas related to 'theory of mind'), and plot following (e.g. the lateral prefrontal cortex), than those who did not have an ASD diagnosis. In contrast, two groups who differed in their degree of autistic traits, but did not have a diagnosis of ASD, showed no significant differences in neural synchrony across the whole brain. These results shed some light on how autistic traits may contribute to an individual's conscious experience of the world, and how, for children with ASD, that experience may differ markedly from that of those without ASD.Very preterm infants are at high risk for motor impairments. Early interventions can improve outcomes in this cohort, but they would be most effective if clinicians could accurately identify the highest-risk infants early. A number of biomarkers for motor development exist, but currently none are sufficiently accurate for early risk-stratification. We prospectively enrolled very preterm (gestational age ≤31 weeks) infants from four level-III NICUs. Structural brain MRI was performed at term-equivalent age. We used a established pipeline to automatically derive brain volumetrics and cortical morphometrics - cortical surface area, sulcal depth, gyrification index, and inner cortical curvature - from structural MRI. We related these objective measures to Bayley-III motor scores (overall, gross, and fine) at two-years corrected age. Lasso regression identified the three best predictive biomarkers for each motor scale from our initial feature set. In multivariable regression, we assessed the independent value of these brain biomarkers, over-and-above known predictors of motor development, to predict motor scores. 75 very preterm infants had high-quality T2-weighted MRI and completed Bayley-III motor testing. All three motor scores were positively associated with regional cortical surface area and subcortical volumes and negatively associated with cortical curvature throughout the majority of brain regions. In multivariable regression modeling, thalamic volume, curvature of the temporal lobe, and curvature of the insula were significant predictors of overall motor development on the Bayley-III, independent of known predictors. Objective brain morphometric biomarkers at term show promise in predicting motor development in very preterm infants.

Insomnia disorder (ID) is a prevalent sleep disorder, which seriously affects people's daily life and was found to be associated with increased frequency of sleep stage shifts. Previous findings had revealed the critical role of the nucleus accumbens (NAc) in sleep-wake transition. However, the neuroimaging studies of the NAc in patients with ID have been rare. We hypothesized that structural and functional abnormalities of the NAc would be implicated in ID.

Twenty-six ID patients and 36 matched healthy controls (HC) were included in the current study. The volumes and corresponding resting-state functional connectivity (RSFC) of the bilateral NAc were compared between the two groups. The abnormal RSFC in ID were then correlated with Pittsburgh Sleep Quality Index (PSQI).

Compared with HC, ID patients showed significantly increased volume of right NAc. Several brain regions showed increased RSFC with the NAc in ID patients, such as medial prefrontal cortex (mPFC), anterior cingulate cortex (ACC), caudate of cognitive function in the patients, respectively. It is hoped that our study focusing on NAc-mPFC circuits could provide new insights for the neural mechanisms of ID and potential novel therapeutic targets for treatment of ID patients.

Increasing evidence indicates the involvement of the GABAergic system in the pathophysiology of hypothyroidism. We aimed to investigate longitudinal changes of brain GABA in primary hypothyroidism before and after levothyroxine (L-T4) treatment.

In 18 patients with hypothyroidism, we used the MEGA-PRESS (Mescher-Garwood point-resolved spectroscopy) editing sequence to measure brain GABA levels from medial prefrontal cortex (mPFC) and posterior cingulate cortex (PCC) at baseline and after 6-months of L-T4 treatment. Sex- and age-matched healthy controls (n=18) were scanned at baseline. Thyroid function and neuropsychological tests were also performed.

GABA signals were successfully quantified from all participants with fitting errors lower than 15%. GABA signal was labeled as GABA+ due to contamination from co-edited macromoleculars and homocarnosine. In hypothyroid patients, mean GABA+ was significantly lower in the mPFC region compared with controls (p=0.031), and the mPFC GABA+ measurements were significantly correlated with depressive symptoms and memory function (r=-0.558, p=0.016; r=0.522, p=0.026, respectively). After adequate L-T4 treatment, the mPFC GABA+ in hypothyroid patients increased to normal level, along with relieved neuropsychological impairments.

The study suggested the decrease of GABA+ may be an important neurobiological factor in the pathophysiology of hypothyroidism. Treatment of L-T4 may reverse the abnormal GABA+ and hypothyroidism-induced neuropsychiatric impairments, indicating the action mode of L-T4 in adjunctive treatment of affective disorders.

The study suggested the decrease of GABA+ may be an important neurobiological factor in the pathophysiology of hypothyroidism. Treatment of L-T4 may reverse the abnormal GABA+ and hypothyroidism-induced neuropsychiatric impairments, indicating the action mode of L-T4 in adjunctive treatment of affective disorders.