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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.Patients diagnosed with disorders of consciousness show minimal or inconsistent behavioural evidence of conscious awareness. However, using functional neuroimaging, recent research in clinical neuroscience has identified a subpopulation of these patients who reliably produce neural markers indicative of awareness. In this study, we recorded electroencephalograms during a response-free movie task to assess narrative processing in patients with disorders of consciousness. Thirteen patients diagnosed with a disorder of consciousness and 28 healthy controls participated in this study. We designed a movie-watching/listening paradigm involving two suspenseful movie clips, one audiovisual and one audio-only, and used electroencephalography to extract patterns of brain activity that were maximally correlated between subjects. These activity patterns served as electrophysiological indices of narrative processing, which were compared to the neural responses of patients during the same movies. Our analysis revealed two patterns of neural activity, one for each movie condition, that were significantly and reliably correlated between healthy participants. Of the twelve patients who watched the audiovisual movie, 25% produced a pattern of activity that was significantly correlated with the healthy group, while of the ten who listened to the audio narrative, 30% produced electrophysiological patterns similar to controls (one patient responded appropriately to both). The method presented here allows for rapid bedside assessment of higher-order cognitive processing in patients with disorders of consciousness. By leveraging the common neural response to movie stimuli, we were able to identify comparable patterns of brain activity in individual, behaviourally non-responsive patients, reflecting a capacity for narrative processing.Parkinson's dementia is a common and devastating part of Parkinson's disease. Whilst timing and severity vary, dementia in Parkinson's is often preceded by visual dysfunction. White matter changes, representing axonal loss, occur early in the disease process. Clarifying which white matter connections are affected in Parkinson's with visual dysfunction and why specific connections are vulnerable will provide important mechanistic insights. Here, we use diffusion tractography in 100 Parkinson's patients (33 low visual performers) and 34 controls to identify patterns of connectivity loss in Parkinson's with visual dysfunction. We examine the relationship between regional transcription and connectivity loss, using the Allen Institute for Brain Science transcriptome atlas. We show that interhemispheric connections are preferentially affected in Parkinson's low visual performers. Interhemispheric connection loss was associated with downweighted genes related to the smoothened signalling pathway (enriched in glutamatergic neurons) and upweighted metabolic genes. Risk genes for Parkinson's but not Alzheimer's or Dementia with Lewy bodies were over-represented in upweighted genes associated with interhemispheric connection loss. Our findings suggest selective vulnerability in Parkinson's patients at highest risk of dementia (those with visual dysfunction), where differences in gene expression and metabolic dysfunction, affecting longer connections with higher metabolic burden, drive connectivity loss.

Disruption of central networks, particularly of those responsible for integrating multimodal afferents in a spatial reference frame, were proposed in the pathophysiology of lateral trunk flexion in Parkinson's disease (PD). Knowledge about the underlying neuroanatomical structures is limited.

To investigate if decreased focal grey matter (GM) is associated with trunk flexion to the side and if the revealed GM clusters correlate with a disturbed perception of verticality in PD.

37 PD patients with and without lateral trunk flexion were recruited. Standardized photos were taken from each patient and trunk orientation was measured by a blinded rater. Voxel-based morphometry (VBM) was used to detect associated clusters of decreased GM. The subjective visual vertical (SVV) was assessed as a marker for perception of verticality and SVV estimates were correlated with GM clusters.

VBM revealed clusters of decreased GM in the right posterior parietal cortex and in the right thalamus were associated with lateral trunk flexion. The SVV correlated with the extent of trunk flexion, and the side of the SVV tilt correlated with the side of trunk flexion. BGB-283 solubility dmso GM values from the thalamus correlated with the SVV estimates.

We report an association between neurodegenerative changes within the posterior parietal cortex and the thalamus and lateral trunk flexion in PD. These brain structures are part of a network proposed to be engaged in postural control and spatial self-perception. Disturbed perception of verticality points to a shifted egocentric spatial reference as an important pathophysiological feature.

We report an association between neurodegenerative changes within the posterior parietal cortex and the thalamus and lateral trunk flexion in PD. These brain structures are part of a network proposed to be engaged in postural control and spatial self-perception. Disturbed perception of verticality points to a shifted egocentric spatial reference as an important pathophysiological feature.Epileptic networks, defined as brain regions involved in epileptic brain activity, have been mapped by functional connectivity in simultaneous electroencephalography and functional magnetic resonance imaging (EEG-fMRI) recordings. This technique allows to define brain hemodynamic changes, measured by the Blood Oxygen Level Dependent (BOLD) signal, associated to the interictal epileptic discharges (IED), which together with ictal events constitute a signature of epileptic disease. Given the highly time-varying nature of epileptic activity, a dynamic functional connectivity (dFC) analysis of EEG-fMRI data appears particularly suitable, having the potential to identify transitory features of specific connections in epileptic networks. In the present study, we propose a novel method, defined dFC-EEG, that integrates dFC assessed by fMRI with the information recorded by simultaneous scalp EEG, in order to identify the connections characterised by a dynamic profile correlated with the occurrence of IED, forming the dynamic epileptic subnetwork.