Risk Factors for Congenital Deafness in Pediatric Patients Who Underwent Otoaccoustic Emission (OAE) and Auditory Brainstem Response (ABR) Examinations in General Hospital Mohammad Hoesin Palembang, Indonesia

Introduction: Congenital deafness is a hearing loss that occurs at birth. Congenital deafness in neonates can be caused by risk factors during pregnancy and during the birth process. The tests carried out for hearing screening for neonates in hospital up to 1 month old are Otoaccoustic Emission (OAE) and Auditory Brainstem Response (ABR) examinations. Objective: Determining the relationship between family history of deafness, syndromes associated with sensorineural hearing loss, TORCH infection and prenatal syphilis, use of ototoxic drugs during pregnancy, prematurity, low birth weight, asphyxia, and hyperbilirubinemia with the incidence of congenital deafness in children Methods: This cross-sectional study was conducted based on medical record datas from children who underwent OAE and ABR examinations at Dr. Mohammad Hoesin Palembang hospital from January 2019 to February 2021. Results: From the 349 children, 180 (51.6%) had bilateral OAE and ABR pass results, 161 (46.1%) had bilateral referrals and 8 (2.3%) children received unilateral refer results. From 122 children with risk factors, 38 (31.1%) children with bilateral passes, 81 (66.4%) children with bilateral referrals and 3 (2.5 %) children with unilateral refer. From 227 children without risk factors, 142 (62.6 %) children with a bilateral pass, 80 (35.2 %) children with bilateral referrals and 5 (2.2%) children with unilateral refer. The most common risk factor was LBW of 41 (11.7%) children. Chi square test and logistic regression analysis results showed a significant relationship between ototoxic drugs during pregnancy and congenital deafness (p = 0.001) with referral results, the value of Odd Ratio (OR) 9.651. Conclusions: There is a significant relationship between risk factors for ototoxic drugs during pregnancy, TORCH and syphilis infection during pregnancy, asphyxia, congenital syndrome, LBWand hyperbilirubinemia with congenital deafness

Reward neurocircuitry predicts longitudinal changes in alcohol use following trauma exposure

Background: Trauma is a risk factor for developing maladaptive alcohol use. Preclinical research has shown that stress alters the processing of midbrain and striatal reward and incentive signals. However, little research has been conducted on alterations in reward-related neurocircuitry post-trauma in humans. Neuroimaging markers may be particularly useful as they can provide insight into the underlying mechanisms that may make an individual more vulnerable to developing trauma-related psychopathologies. This study aimed to identify reward-related neural mechanisms associated with changes in alcohol use after trauma exposure. Methods: Participants were recruited from U.S. emergency departments (ED) for the AURORA study (N=286, 178 female). Trauma-related change in alcohol use at 8 weeks post-trauma relative to pre-trauma was quantified as a change in 30-day total drinking per the PhenX Toolkit Alcohol 30-Day Quantity and Frequency Measure. Reward-related neurocircuitry activation and functional connectivity (FC) were assessed 2 weeks post-trauma using fMRI during a monetary reward task using region of interest and whole-brain voxelwise analyses. Results: Greater increase in alcohol use from pre-trauma to 8 weeks post-trauma was predicted by (1) greater ventral tegmental area (VTA) and (2) greater cerebellum activation during Gain>Loss trials measured 2 weeks post-trauma and (3) greater seed-based FC between the VTA and lateral occipital cortex and precuneus. Conclusions: Altered VTA activation and FC early post-trauma could predict reward-seeking and processing, contributing to greater alcohol use post-trauma. These data provide novel evidence of neural mechanisms that underlie increased alcohol use early post-trauma that can be targeted via early interventions to the development of maladaptive alcohol use

ENIGMA-Meditation: Worldwide consortium for neuroscientific investigations of meditation practices

Meditation is a family of ancient and contemporary contemplative mind-body practices that can modulate psychological processes, awareness, and mental states. Over the last 40 years, clinical science has manualised meditation practices and designed various meditation interventions (MIs), that have shown therapeutic efficacy for disorders including depression, pain, addiction, and anxiety. Over the past decade, neuroimaging has examined the neuroscientific basis of meditation practices, effects, states, and outcomes for clinical and non-clinical populations. However, the generalizability and replicability of current neuroscientific models of meditation are yet to be established, as they are largely based on small datasets entrenched with heterogeneity along several domains of meditation (e.g., practice types, meditation experience, clinical disorder targeted), experimental design, and neuroimaging methods (e.g., preprocessing, analysis, task-based, resting-state, structural MRI). These limitations have precluded a nuanced and rigorous neuroscientific phenotyping of meditation practices and their potential benefits. Here, we present ENIGMA-Meditation, the first worldwide collaborative consortium for neuroscientific investigations of meditation practices. ENIGMA-Meditation will enable systematic meta- and mega-analyses of globally distributed neuroimaging datasets of meditation using shared, standardized neuroimaging methods and tools to improve statistical power and generalizability. Through this powerful collaborative framework, existing neuroscientific accounts of meditation practices can be extended to generate novel and rigorous neuroscientific insights, accounting for multi-domain heterogeneity. ENIGMA-Meditation will inform neuroscientific mechanisms underlying therapeutic action of meditation practices on psychological and cognitive attributes, advancing the field of meditation and contemplative neuroscience

Associations of alcohol and cannabis use with change in posttraumatic stress disorder and depression symptoms over time in recently trauma-exposed individuals

BACKGROUND: Several hypotheses may explain the association between substance use, posttraumatic stress disorder (PTSD), and depression. However, few studies have utilized a large multisite dataset to understand this complex relationship. Our study assessed the relationship between alcohol and cannabis use trajectories and PTSD and depression symptoms across 3 months in recently trauma-exposed civilians. METHODS: In total, 1618 (1037 female) participants provided self-report data on past 30-day alcohol and cannabis use and PTSD and depression symptoms during their emergency department (baseline) visit. We reassessed participant\u27s substance use and clinical symptoms 2, 8, and 12 weeks posttrauma. Latent class mixture modeling determined alcohol and cannabis use trajectories in the sample. Changes in PTSD and depression symptoms were assessed across alcohol and cannabis use trajectories via a mixed-model repeated-measures analysis of variance. RESULTS: Three trajectory classes (low, high, increasing use) provided the best model fit for alcohol and cannabis use. The low alcohol use class exhibited lower PTSD symptoms at baseline than the high use class; the low cannabis use class exhibited lower PTSD and depression symptoms at baseline than the high and increasing use classes; these symptoms greatly increased at week 8 and declined at week 12. Participants who already use alcohol and cannabis exhibited greater PTSD and depression symptoms at baseline that increased at week 8 with a decrease in symptoms at week 12. CONCLUSIONS: Our findings suggest that alcohol and cannabis use trajectories are associated with the intensity of posttrauma psychopathology. These findings could potentially inform the timing of therapeutic strategies