Nightmares in Children with Foetal Alcohol Spectrum Disorders, Autism Spectrum Disorders, and Their Typically Developing Peers

Children with Foetal Alcohol Spectrum Disorders (FASD) and Autism Spectrum Disorders (ASD) experience significantly higher rates of sleep disturbances than their typically developing (TD) peers. Pre-sleep anxiety and waking emotional content is known to affect the content and frequency of nightmares, which can be distressing to children and caregivers. This is the first study to analyse nightmare frequency and content in FASD, and to assess its association with psychometric outcomes. Using online caregiver questionnaires, we assessed reports from 277 caregivers of children with ASD (n = 61), FASD (n = 112), and TD children (n = 104) using the Children’s Sleep Habits Questionnaire (CSHQ), the Child Behaviour Checklist (CBCL), the Spence Children’s Anxiety Scale (SCAS), and the Behaviour Rating Inventory for Executive Functioning (BRIEF). Within the ASD group, 40.3% of caregivers reported their children had nightmares. Within the FASD group, 73.62% of caregivers reported their children had nightmares, and within the TD group, 21.36% of caregivers reported their children had nightmares. Correlation analysis revealed significant associations between anxiety and nightmares, maladaptive behaviour and nightmares, and executive functioning and nightmares in the TD and FASD groups, but not ASD group. This paper adds to the emerging body of work supporting the need for sleep interventions as part of clinical practice with regard to children with ASD and FASD. As a relatively niche but important area of study, this warrants much needed further research.

Thinner retinal nerve fibre layer in young adults with foetal alcohol spectrum disorders

Background/AimsOphthalmological abnormalities such as ptosis, strabismus, refractive errors and optic nerve hypoplasia have been reported in foetal alcohol spectrum disorders (FASD). The purpose of this study was to investigate whether retinal thickness, retinal nerve fibre layer (RNFL) and optic disc area (ODA) differ between individuals with FASD and healthy controls.MethodsBest-corrected visual acuity (BCVA) in terms of logarithm of the minimum angle of resolution (logMAR), refraction, and fundus variables measured by optical coherence tomography were obtained from 26 young adults with FASD (12 women, median age 23 years) and 27 controls (18 women, median age 25 years).ResultsThe total thickness of the peripapillary RNFL was significantly lower in the FASD group than in controls; median (range) in the right/left eye was 96.5 (60–109)/96 (59–107) µm in the FASD group and 105 (95–117)/103 (91–120) µm among controls (p=0.001 and p=0.0001). Macular RNFL and retinal thickness measurements from the FASD group were also lower in most of the nine ETDRS areas, except for the central parts. Median (range) BCVA in the best eye was 0.00 (−0.1–0.3) logMAR in the FASD group and 0.00 (−0.2–0.0) logMAR in controls (p=0.001). No significant differences between the groups were found regarding ODA or refraction.ConclusionSignificant differences in peripapillary and macular RNFL, retinal thickness and BCVA were found in this group of young adults with FASD compared with healthy controls. However, there were no differences in the size of the optic disc.

Histone deacetylases inhibitor trichostatin A reverses anxiety-like symptoms and memory impairments induced by maternal binge alcohol drinking in mice

Background:Alcohol exposure during development has detrimental effects, including a wide range of physical, cognitive and neurobehavioural anomalies known as foetal alcohol spectrum disorders. However, alcohol consumption among pregnant woman is an ongoing latent health problem.Aim:In the present study, the effects of trichostatin A (TSA) on emotional and cognitive impairments caused by prenatal and lactational alcohol exposure were assessed. TSA is an inhibitor of class I and II histone deacetylases enzymes (HDAC), and for that, HDAC4 activity was determined. We also evaluated mechanisms underlying the behavioural effects observed, including the expression of brain-derived neurotrophic factor (BDNF) in discrete brain regions and newly differentiated neurons in the dentate gyrus (DG).Methods:C57BL/6 female pregnant mice were used, with limited access to a 20% v/v alcohol solution as a procedure to model binge alcohol drinking during gestation and lactation. Male offspring were treated with TSA during the postnatal days (PD28–35) and behaviourally evaluated (PD36–55).Results:Early alcohol exposure mice presented increased anxiogenic-like responses and memory deterioration – effects that were partially reversed with TSA. Early alcohol exposure produces a decrease in BDNF levels in the hippocampus (HPC) and prefrontal cortex, a reduction of neurogenesis in the DG and increased activity levels of the HDAC4 in the HPC.Conclusions:Such findings support the participation of HDAC enzymes in cognitive and emotional alterations induced by binge alcohol consumption during gestation and lactation and would indicate potential benefits of HDAC inhibitors for some aspects of foetal alcohol spectrum disorders.

Long-term epigenetic changes in offspring mice exposed to alcohol during gestation and lactation

Background: Alcohol exposure impairs brain development and leads to a range of behavioural and cognitive dysfunctions, termed as foetal alcohol spectrum disorders. Although different mechanisms have been proposed to participate in foetal alcohol spectrum disorders, the molecular insights of such effects are still uncertain. Using a mouse model of foetal alcohol spectrum disorder, we have previously shown that maternal binge-like alcohol drinking causes persistent effects on motor, cognitive and emotional-related behaviours associated with neuroimmune dysfunctions. Aims: In this study, we sought to evaluate whether the long-term behavioural alterations found in offspring with early exposure to alcohol are associated with epigenetic changes in the hippocampus and prefrontal cortex. Methods: Pregnant C57BL/6 female mice underwent a model procedure for binge alcohol drinking throughout both the gestation and lactation periods. Subsequently, adult offspring were assessed for their cognitive function in a reversal learning task and brain areas were extracted for epigenetic analyses. Results: The results demonstrated that early binge alcohol exposure induces long-term behavioural effects along with alterations in histone acetylation (histone H4 lysine 5 and histone H4 lysine 12) in the hippocampus and prefrontal cortex. The epigenetic effects were linked with an imbalance in histone acetyltransferase activity that was found to be increased in the prefrontal cortex of mice exposed to alcohol. Conclusions: In conclusion, our results reveal that maternal binge-like alcohol consumption induces persistent epigenetic modifications, effects that might be associated with the long-term cognitive and behavioural impairments observed in foetal alcohol spectrum disorder models.