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Aim: Prenatal exposure to cigarettes leads to alterations in brain development during pregnancy. This has an impact on postnatal psychological and behavioural processes, affecting an infant's neurobehavioural profile with little known about which aspects are affected. The evidence was synthesised to assess the effects of prenatal cigarette smoke exposure on neurobehavioural outcomes within the first year of life.Methods: Six databases were searched (Web of Science Core Collections, MEDLINE, PsycINFO, CINAHL, EBSCOhost eBook Collection and OpenGrey) in November 2018. Eligible studies (n = 17) had to include a measure of prenatal cigarette exposure and a neurobehavioural assessment ≤1 year of age.Results: In the first year of life, specific areas of neurobehavioural functioning are related to prenatal cigarette exposure with eight out of 10 areas of neurobehaviour having significant medium (negative affect, attention, excitability, irritability and orientation) or small (muscle tone, regulation and difficult temperament) pooled effect sizes. Only lethargy and stress did not show any significant pooled effects.Conclusion: Prenatal cigarette exposure affects a significant range of behaviours during the first year of life. [ABSTRACT FROM AUTHOR]

Maternal weight before and during pregnancy is associated with offspring neurobehaviour in childhood. We investigated maternal weight prior to and during pregnancy in relation to neonatal neurobehaviour. We hypothesized that maternal obesity and excessive gestational weight gain would be associated with poor neonatal attention and affective functioning. Participants ( n = 261) were recruited, weighed and interviewed during their third trimester of pregnancy. Pre-pregnancy weight was self-reported and validated for 210 participants, with robust agreement with medical chart review ( r = 0.99). Neurobehaviour was measured with the NICU Network Neurobehavioural Scale (NNNS) administered on Days 2 and 32 postpartum. Maternal exclusion criteria included severe or persistent physical or mental health conditions (e.g. chronic disease or diagnoses of Bipolar Disorder or Psychotic Spectrum Disorders), excessive substance use, and social service/foster care involvement or difficulty understanding English. Infants were from singleton, full-term (37-42 weeks gestation) births with no major medical concerns. Outcome variables were summary scores on the NNNS ( n = 75-86). For women obese prior to pregnancy, those gaining in excess of Institute of Medicine guidelines had infants with poorer regulation, lower arousal and higher lethargy. There were no main effects of maternal pre-pregnancy body mass index on neurobehaviour. Women gaining above Institute of Medicine recommendations had neonates with better quality of movement. Additional studies to replicate and extend results past the neonatal period are needed. Results could support underlying mechanisms explaining associations between maternal perinatal weight and offspring outcomes. These mechanisms may inform future prevention/intervention strategies. © 2016 Blackwell Publishing Ltd [ABSTRACT FROM AUTHOR]

A tremendous increase has been documented in the recent past in prescribing second generation atypical antipsychotic drugs (AAPDs) to the pregnant women with psychosis, considering their reproductive and teratogenic safety. Among AAPDs, risperidone (RIS) ranked third after olanzapine (OLZ) and quetiapine (QUE) used during pregnancy, as OLZ is associated to substantial weight gain in adults and offspring. Although teratogenic safety of RIS has been established, its potential role in developmental neurotoxicity and related neurobehavioral impairments in adolescents has not been documented so far. Therefore, present study has been undertaken to elucidate the effect of prenatal exposure to risperidone (RIS) on developmental neurotoxicity and apoptotic neurodegeneration in neocortical region of fetal brain; and related functional sequelae in young rat offspring. The pregnant Wistar rats were exposed to RIS at 0.8, 1.0 and 2.0 mg/kg, at equivalent therapeutic doses, orally from GD 6 to 21. Half of the pregnant rats were sacrificed and their brains were collected, weighed, and processed for neurohistopathological and apoptotic neurodegenerative evaluation. The remaining dams were allowed to deliver naturally, and their offspring were reared up to 10 weeks for neurobehavioral study. Prenatal exposure to RIS induced significant stunting of fetal body and brain weight, substantial reduction in the thickness of neocortical layers and apoptotic neurodegeneration in fetal brains, and delayed postnatal development and growth of the offspring; as well as long- lasting impact on anxiety like impaired behavioral responses on explorative mazes. Therefore, health care providers should be careful in prescribing atypical antipsychotics in general and RIS in particular, to the pregnant psychotic population. [ABSTRACT FROM AUTHOR]

To facilitate investigation of diverse rodent behaviours in rodents' home cages, we have developed an integrated modular platform, the Smart Cage™ system ( Afa Sci, Inc. Burlingame, CA, USA), which enables automated neurobehavioural phenotypic analysis and in vivo drug screening in a relatively higher-throughput and more objective manner., The individual platform consists of an infrared array, a vibration floor sensor and a variety of modular devices. One computer can simultaneously operate up to 16 platforms via USB cables., The Smart Cage™ detects drug-induced increases and decreases in activity levels, as well as changes in movement patterns. Wake and sleep states of mice can be detected using the vibration floor sensor. The arousal state classification achieved up to 98% accuracy compared with results obtained by electroencephalography and electromyography. More complex behaviours, including motor coordination, anxiety-related behaviours and social approach behaviour, can be assessed using appropriate modular devices and the results obtained are comparable with results obtained using conventional methods., In conclusion, the Smart Cage™ system provides an automated and accurate tool to quantify various rodent behaviours in a 'stress-free' environment. This system, combined with the validated testing protocols, offers powerful a tool kit for transgenic phenotyping and in vivo drug screening. [ABSTRACT FROM AUTHOR]

Aim: This study explored inter-rater reliability, discriminative, construct and predictive validity of the Neurobehavioral Assessment of the Preterm Infant (NAPI) in a gestational-age-based cohort. Methods: The NAPI was conducted at 35 weeks post-menstrual age for 170 infants born <32 weeks. Cognitive and motor development was assessed at 2 years using the Mental Development Index (MDI) and Psychomotor Development Index (PDI) of Bayley Scales of Infant Development-II for 159 infants. Results: Only NAPI motor and irritability scores were significantly different between very (29-3 w) and extremely preterm (<28 w) infants. Results regarding construct validity were variable: there were weak correlations between NAPI motor scores and gestational age (r = −0.23; p = 0.003), days in NICU (r = −0.24; p = 0.001); NAPI alertness scores and days in NICU (r = −0.16; p = 0.037); and NAPI irritability scores and gestational age (r = 0.21; p = 0.006). There were no significant associations with other markers of adverse outcome. Only NAPI irritability scores were correlated with MDI scores (r = −0.16; p = 0.040) but accounted for little additional variance after adjustment for neonatal factors (ΔR2 = 0.035; p = 0.012). Conclusion: We found little evidence of the utility of the NAPI as a measure of short-term neurobehavioural function or for predicting neurodevelopmental outcomes in very preterm infants. It may have greater predictive power when used serially to detect delayed neurobehavioural maturation. [ABSTRACT FROM AUTHOR]

To facilitate investigation of diverse rodent behaviours in rodents' home cages, we have developed an integrated modular platform, the Smart Cage™ system ( Afa Sci, Inc. Burlingame, CA, USA), which enables automated neurobehavioural phenotypic analysis and in vivo drug screening in a relatively higher-throughput and more objective manner., The individual platform consists of an infrared array, a vibration floor sensor and a variety of modular devices. One computer can simultaneously operate up to 16 platforms via USB cables., The Smart Cage™ detects drug-induced increases and decreases in activity levels, as well as changes in movement patterns. Wake and sleep states of mice can be detected using the vibration floor sensor. The arousal state classification achieved up to 98% accuracy compared with results obtained by electroencephalography and electromyography. More complex behaviours, including motor coordination, anxiety-related behaviours and social approach behaviour, can be assessed using appropriate modular devices and the results obtained are comparable with results obtained using conventional methods., In conclusion, the Smart Cage™ system provides an automated and accurate tool to quantify various rodent behaviours in a 'stress-free' environment. This system, combined with the validated testing protocols, offers powerful a tool kit for transgenic phenotyping and in vivo drug screening. [ABSTRACT FROM AUTHOR]

Objective: Infant cry characteristics reflect the neurological and medical status of the infant. This study compared the acoustic cry characteristics of infants born to mothers maintained on methadone during pregnancy with those of infants not exposed to methadone during pregnancy. Methods: At 42 weeks of post-menstrual age, 89 crying episodes ranging in duration from 1.15 to 1.97 sec were collected from 10 methadone-exposed (ME) and 10 non-methadone-exposed (NE) infants. Cry utterances were analysed acoustically using spectrographic displays and measures of cry utterance duration and fine-grained analyses of the fundamental frequency calculated for each cry. Results: No between-group differences were found on measures of cry duration or fundamental frequency. However, analyses of frequency perturbation showed that the cry utterances of ME infants were characterized by significantly higher levels of frequency perturbation than the cries of infants not exposed to methadone. These effects largely persisted after statistical control for the confounding effects of other maternal drug use during pregnancy. Conclusion: The crying behaviour of infants exposed prenatally to the synthetic opiate, methadone, is characterized by higher levels of vocal fold vibratory perturbation than NE infants. These findings suggest the possibility of early, subtle neurological vulnerability in this high-risk group of infants. [ABSTRACT FROM AUTHOR]

This is the first published case description in the current literature of the association of definite Gilles de la Tourette syndrome (GTS) and the Smith–Magenis syndrome (SMS), both confirmed by DSM-IV-TR criteria and molecular cytogenetic analysis, respectively. The co-occurrence of GTS, SMS and their common behavioural/neuropsychiatric abnormalities should warrant further genetic investigation of chromosome 17p11.2 deletion site as it may be a promising region for containing a gene(s) of aetiological importance in the development of the GTS phenotype. Alternatively, the co-occurrence may be due to the common endophenotypic mechanisms shared by these disorders, rather than being specific for GTS that could be explored using strategies of quantitative trait loci – endophenotype-based approach. Research into this genomic region may also benefit psychiatric genetic research in enhancing understanding of the biological and molecular underpinnings of common behavioural problems that are seen in both GTS and SMS. This would lead to advancement in neurobehavioural/neuropsychiatric genetics which will help in further explaining the broader perspective of gene–brain–behaviour interrelationships. [ABSTRACT FROM AUTHOR]

Adolescent brain development seems to be important for the maturation of brain structures and behaviour. Intermittent binge ethanol drinking is common among adolescents, and this type of drinking can induce brain damage. Because we have demonstrated that chronic ethanol treatment induces inflammatory processes in the brain, we investigate whether intermittent ethanol intoxication enhances cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in adolescent rats, and whether these mediators induce brain damage and cause permanent cognitive dysfunctions. Adolescent rats were exposed to ethanol (3.0 g/kg) for two consecutive days at 48-h intervals over 14 days. Levels of COX-2, iNOS and cell death were assessed in the neocortex, hippocampus and cerebellum 24 h after the final ethanol administration. The following day or 20 days after the final injection (adult stage), animals were tested for different behavioural tests (conditional discrimination learning, rotarod, object recognition, beam-walking performance) to assess cognitive and motor functions. Our results show that intermittent ethanol intoxication upregulates COX-2 and iNOS levels, and increases cell death in the neocortex, hippocampus and cerebellum. Furthermore, animals treated with ethanol during adolescence exhibited behavioural deficits that were evident at the end of ethanol treatments and at the adult stage. Administration of indomethacin, a COX-2 inhibitor, abolishes the induction of COX-2 and iNOS expression and cell death, preventing ethanol-induced behavioural deficits. These findings indicate that binge pattern exposure to ethanol during adolescence induces brain damage by inflammatory processes and causes long-lasting neurobehavioural consequences. Accordingly, administering indomethacin protects against ethanol-induced brain damage and prevents detrimental ethanol effects on cognitive and motor processes. [ABSTRACT FROM AUTHOR]