Brain oscillatory patterns of affective prosody perception in children with autism spectrum disorder
Background
Paralinguistic features, such as prosody (tempo, loudness, and timbre), are an essential marker of a speaker’s emotional state. Abnormal processing of emotional prosody may result in the deficient social behavior associated with autism spectrum disorder (ASD).
Method
Two groups of children participated in our study: the ASD group consisted of 30 preschoolers from 4 to 6 years of age and 24 typically developing (TD) peers. An electroencephalogram (EEG) was acquired in response to a combination of syllables uttered with the following types of emotional prosody: joy, anger, sadness, fear, and calmness.
Results
Children with ASD and TD showed a similar EEG oscillatory response to fear and anger prosodies. Significant group differences in power spectral density (PSD) were detected for sad and joy intonations. The PSD differences between pairs of intonations, such as joyful and sad, sad and neutral, or joyful and neutral, were significantly higher in the control group than in the ASD group. EEG responses to affective prosody also demonstrated less hemispheric asymmetry in the ASD than in the TD group.
Conclusions
Our results suggest that difficulties in emotional prosody recognition in autistic children could be based on the atypical processing of specific acoustic features coding differences between sad, neutral, and joyful intonations and could underlie emotional perception deficits in individuals with ASD.
Background: The hypothalamic-pituitary-adrenal (HPA) axis, inflammatory processes and neurotrophic factor systems are involved in pathogenesis of both epilepsy and depressive disorders. The study aimed to explore these systems in patients with focal epilepsy (PWE, n = 76), epilepsy and comorbid depression (PWCED n = 48), and major depressive disorder (PWMDD, n = 62) compared with healthy controls (HC, n = 78). Methods: Parameters of the HPA axis, neurotrophic factors, and TNF-α were measured in blood serum along with the hemogram. Results: Serum cortisol level was augmented in PWE, PWCED, and PWMDD compared with HC and was higher in PWMDD than in PWE. Serum cortisol negatively correlated with Mini–Mental State Examination (MMSE) score in PWE, and positively with depression inventory–II (BDI-II) score in PWMDD. Only PWMDD demonstrated elevated plasma ACTH. Serum TNF-α, lymphocytes, and eosinophils were augmented in PWMDD; monocytes elevated in PWE and PWCED, while neutrophils were reduced in PWE and PWMDD. Serum BDNF was decreased in PWE and PWCED, CNTF was elevated in all groups of patients. In PWE, none of above indices depended on epilepsy etiology. Conclusions: The results confirm the involvement of HPA axis and inflammatory processes in pathogenesis of epilepsy and depression and provide new insights in mechanisms of epilepsy and depression comorbidity.
This work aimed to study the recovery of consciousness during forced awakening from slow-wave sleep (SWS) and rapid eye movement sleep (REM) in healthy volunteers. To track the changes in the degree of awareness of the stimuli during the transition to wakefulness, event-related potentials (ERPs) and motor responses (MR) in the auditory local-global paradigm were analyzed. The results show that during awakening from both SWS and REM, first, alpha-activity restores in the EEG, and only 20 and 25 s (for REM and SWS awakenings, respectively) after alpha onset MR to target stimuli recovers. During REM awakening, alpha-rhythm, MR, and conscious awareness of stimuli recover faster than during SWS awakening. Moreover, pre-attentive processing of local irregularities emerges earlier, even before alpha-rhythm onset, while during SWS awakening, the local effect we registered only after alpha restoration. The P300-like response both on global and local irregularities was found only when accurate MR was restored. Thus, the appearance in EEG predominating alpha-activity is insufficient either for conscious awareness of external stimuli or for generating MR to them. This work may help to understand the pathophysiology of sleep disorders well as conditions characterized by the dissociation between behavior and various aspects of consciousness.
We performed RNA sequencing of the dorsal and ventral parts of the hippocampus and compared it with previously published data to determine the differences in the dorsoventral gradients of gene expression that may result from biological or technical variability. Our data suggest that the dorsal and ventral parts of the hippocampus differ in the expression of genes related to signaling pathways mediated by classical neurotransmitters (glutamate, GABA, monoamines, etc.) as well as peptide and Wnt ligands. These hippocampal parts also diverge in the expression of axon-guiding molecules (both receptors and ligands) and splice isoforms of genes associated with intercellular signaling and cell adhesion. Furthermore, analysis of differential expressions of genes specific for astrocytes, microglia, oligodendrocytes, and vascular cells suggests that non-neuronal cells may also differ in the characteristics between hippocampal parts. Analysis of expression of transposable elements showed that depletion of ribosomal RNA strongly increased the representation of transposable elements in the RNA libraries and helped to detect a weak predominance of expression of these elements in the ventral hippocampus. Our data revealed new molecular dimensions of functional differences between the dorsal and ventral hippocampus and points to possible cascades that may be involved in the longitudinal organization of the hippocampus.