Mindfulness is a form of meditation based on the Buddhist tradition, which has been used over the last two decades to successfully treat a multitude of mental health problems. Bringing mindfulness into parenting (“mindful parenting”) is one of the applications of mindfulness. Mindful parenting interventions are increasingly being used to help prevent and treat mental disorders in children, parenting problems, and prevent intergenerational transmission of mental disorders from parents to children. However, to date, few studies have examined the hypothesized mechanisms of change brought about by mindful parenting. We discuss six possible mechanisms through which mindful parenting may bring about change in parent–child interactions in the context of child and parent mental health problems. These mechanisms are hypothesized to be mediated by the effects of mindfulness on parental attention by: (1) reducing parental stress and resulting parental reactivity; (2) reducing parental preoccupation resulting from parental and/or child psychopathology; (3) improving parental executive functioning in impulsive parents; (4) breaking the cycle of intergenerational transmission of dysfunctional parenting schemas and habits; (5) increasing self-nourishing attention; and (6) improving marital functioning and co-parenting. We review research that has applied mindful parenting in mental health settings, with a focus on evidence for these six mechanisms. Finally, we discuss directions for future research into mindful parenting and the crucial questions that this research should strive to answer.

Darwin originally pointed out that there is something about infants which prompts adults to respond to and care for them, in order to increase individual fitness, i.e. reproductive success, via increased survivorship of one's own offspring. Lorenz proposed that it is the specific structure of the infant face that serves to elicit these parental responses, but the biological basis for this remains elusive. Here, we investigated whether adults show specific brain responses to unfamiliar infant faces compared to adult faces, where the infant and adult faces had been carefully matched across the two groups for emotional valence and arousal, as well as size and luminosity. The faces also matched closely in terms of attractiveness. Using magnetoencephalography (MEG) in adults, we found that highly specific brain activity occurred within a seventh of a second in response to unfamiliar infant faces but not to adult faces. This activity occurred in the medial orbitofrontal cortex (mOFC), an area implicated in reward behaviour, suggesting for the first time a neural basis for this vital evolutionary process. We found a peak in activity first in mOFC and then in the right fusiform face area (FFA). In mOFC the first significant peak (p<0.001) in differences in power between infant and adult faces was found at around 130 ms in the 10–15 Hz band. These early differences were not found in the FFA. In contrast, differences in power were found later, at around 165 ms, in a different band (20–25 Hz) in the right FFA, suggesting a feedback effect from mOFC. These findings provide evidence in humans of a potential brain basis for the “innate releasing mechanisms” described by Lorenz for affection and nurturing of young infants. This has potentially important clinical applications in relation to postnatal depression, and could provide opportunities for early identification of families at risk.

AIM This systematic review aimed to pull together the findings from research into behavioural systems and attention in children with neurofibromatosis type 1 (NF1) and to identify areas that need further study.METHOD Relevant papers were identified through searches of electronic databases (MEDLINE, PsycINFO, EMBASE) and manual searches through reference lists. In total, 5746 articles were identified and 57 met the inclusion criteria. The data were synthesized using the narrative approach, as the studies varied considerably in terms of participants and measures. RESULTSThe results of the review showed that intelligence, academic skills, visuospatial skills, social competence, and attention are impaired in children with NF1. Evidence of deficits in memory, motor functioning, language, and executive functions was less clear. INTERPRETATIONResearch has made marked progress in outlining the behavioural phenotype of NF1. However, although the general areas of impairment are becoming better known, the exact nature of the impairment is still not understood in many areas of behaviour. Care needs to be taken with the way in which behavioural constructs are defined and measured, and the variability of problems in NF1 is a particular challenge. Nevertheless, research is steadily moving towards comprehensive understanding of behaviour in children with NF1.Neurofibromatosis type 1 (NF1) is one of the most common genetic disorders with a prevalence in the UK of 1 per 4560 live births. 1 The main disease feature in childhood is the emergence of multiple café-au-lait spots (flat coffee-coloured skin lesions) and skinfold freckling. The most common complications in childhood are different deficits of cognition and behaviour, which affect the majority of children with NF1. Children with NF1 are also at a higher risk of a number of much rarer physical complications that can affect virtually every system of the body 2 and include disfiguring plexiform neurofibromas, scoliosis, pseudarthrosis, and optic nerve gliomas.The cognitive and behavioural problems associated with NF1 are a major impairment to children's functioning at school and are issues that repeatedly come up in clinical practice as causing great distress to parents. The IQ of children with NF1 is usually within the normal range although somewhat lower than that of their unaffected siblings or community comparisons. More than 70% of children with NF1 perform more poorly at school than would be expected given their intellectual abilities.3 Furthermore, only a small proportion of children with NF1 are diagnosed with attention-deficit-hyperactivity disorder (ADHD), 4 although experimental studies using clinical diagnostic criteria for ADHD suggest that the incidence of this disorder among children with NF1 is up to 40 to 50%. 3 Issues concerning learning and various behaviour problems (such as difficulties with attention, peer relationships, and challenging behaviours) are among the most common complaints by parents of children with NF1 that emerge in our clinic work. Questi...

AIM To investigate psychopathology in children with neurofibromatosis type 1 (NF1), particularly the prevalence of autism spectrum disorder (ASD) and attention-deficit-hyperactivity disorder (ADHD) symptomatology, using a population-based sampling approach.METHOD Standard questionnaire screen reports were analysed for ASD (Social Responsiveness Scale, SRS), ADHD (Conners' Parent Rating Scale-Revised, CPRS-R), and other psychiatric morbidity (Strengths and Difficulties Questionnaire, SDQ) from parents and teachers of children aged from 4 to 16 years (112 females, 95 males) on the UK North West Regional Genetic Service register for NF1.RESULTS Parental response rate was 52.7% (109 ⁄ 207 children; 59 females, 50 males, mean age 9y 11mo, SD 3y 3mo). The SRS showed that in 29.4% (32 ⁄ 109) of children, autism was in the severe, clinical range (T-score>75) and in 26.6% (29 ⁄ 109) in the mild to moderate range (T-score 60-75). CPRS-R scores showed that in 53.8% (57 ⁄ 106) of children autism was in the clinical ADHD range (ADHD index T-score>65). Based on their scores on the SDQ total difficulties scale, 41.5% (44 ⁄ 106) of children were in the abnormal range and 14.2% (15 ⁄ 106) were in the borderline range. Twentyfive per cent (26 ⁄ 104) of children met criteria for both clinical autism and ADHD.INTERPRETATION This representative population-based sample of children with NF1 indicates a high prevalence of ASD symptoms associated with NF1 as well as substantial co-occurrence with ADHD symptoms. The findings clarify the psychopathology of NF1 and show the disorder as a potentially important single-gene cause for autism symptoms.Neurofibromatosis type 1 (NF1) is a common autosomal dominant genetic disorder with a birth incidence of at least one in 2699 and a prevalence of one in 4560.1 Fifty per cent of cases are inherited while the rest are sporadic cases due to spontaneous mutation of the gene located on chromosome 17 (17q11.2). The diagnosis of NF1 is clinical and is based on distinctive cutaneous features of the physical phenotype, such as café-au-lait spots, skinfold freckling, and neurofibromas. The most common associated complication of NF1 in childhood relates to cognitive dysfunction: approximately 80% of children with NF1 experience moderate to severe impairment in one or more areas of cognitive functioning.2 Associated psychiatric morbidity has commonly been reported in NF1, but prevalence estimates have previously been wholly based on clinic referral populations and relatively small samples. Since it is well recognized that clinic referral bias will distort co-occurrence or comorbidity estimation, 3,4 inferences from these studies to the general population of NF1 are insecure. Also, the studies have generally not considered threats to the specificity of any conclusions, for instance that the disturbance found might be a non-specific effect of learning disability or other aspects of developmental disorder.Nevertheless, with these caveats, Samuelsson and Riccardi 5 found significant mental illness in 33% (n=15 ⁄...

WHAT'S KNOWN ON THIS SUBJECT: NF1 is the commonest singlegene neurodevelopmental disorder with known neurobiology and developmental impact on attention and cognition. Its impact on social functioning is described but poorly understood, with no population-based study of autism spectrum disorder (ASD) prevalence in the disorder. WHAT THIS STUDY ADDS:This epidemiological study shows high prevalence of 25% ASD in NF1 not explained by learning difficulties. ASD should be considered during clinical practice with NF1. Further research into NF1 as a single-gene model of ASD is warranted.abstract OBJECTIVE: To determine the prevalence of autism spectrum disorder (ASD) in Neurofibromatosis Type 1 (NF1). METHODS:Second-phase population-based epidemiologic study using an allcase NF1 registry in a defined UK 4.1 million population area. A total of 109 (52.7%) of 207 responders from the initial screening phase were grouped by using the parent-rated Social Responsiveness Scale (SRS) as significant ASD (SRS$76; n 5 32), moderate ASD (SRS $ 60,76; n 5 29), or non-ASD (SRS ,60, n 5 48). Twenty-three cases from the significant ASD group, 16 from moderate ASD, and 8 from non-ASD (total n 5 47), invited proportionately by random selection, were seen for detailed confirmatory ascertainment. Assessments on Autism Diagnostic Interview-Revised, Autism Diagnostic Observation Scale-Generic, and verbal IQ were combined by using standard Collaborative Program for Excellence in Autism criteria into an ASD categorization for each case (ASD, broad ASD with partial features, non-ASD). A preplanned weighted analysis was used to derive prevalence estimates for the whole population.RESULTS: Fourteen (29.5%) of 47 showed ASD, 13 (27.7%) broad ASD, and 20 (42.5%) non-ASD. The ASD/broad ASD group showed male predominance (1.7:1.0), but did not differ significantly from the non-ASD group on IQ, age, socioeconomic status, inheritance, physical severity, or education. The population prevalence estimate is 24.9% ASD (95% confidence interval 13.1%-42.1%) and 20.8% broad ASD (95% confidence interval 10.0%-38.1%); a total of 45.7% showing some ASD spectrum phenotype. Dr Garg contributed to the study design, identified the participants, led the study fieldwork, undertook preliminary analysis, and drafted the initial manuscript and revisions; Professor Green conceptualized the study, contributed to the design, supervised the fieldwork and early analysis, and critically reviewed and revised the manuscript; Dr Leadbitter contributed to the fieldwork assessments, data entry, and initial analysis, and contributed to drafting and critical review of the manuscript; Dr Emsley designed and carried out the analysis, and contributed to the drafting and critical review of the manuscript; Dr Lehtonen contributed to the initial design and patient identification; Dr Evans contributed to the initial design, supervised patient identification, and contributed to drafting and critical review of the manuscript; Dr Huson conceptualized the study, contributed to the design, super...

Postnatal depression and anxiety have been shown to increase the risk of disturbances in mother–child interaction and child development. Research into mechanisms has focused on genetics and maternal behavior; maternal cognitions have received little attention. Our aim was to experimentally determine if worry and rumination in mothers with generalized anxiety disorder (GAD) and major depressive disorder (MDD), diagnosed in the postnatal 6 months, interfered with maternal responsiveness to their 10-month old infants. Mothers (N = 253: GAD n = 90; MDD n = 57; control n = 106) and their infants were randomized to either a worry/rumination prime (WRP) or a neutral prime (NP); mother–infant interactions were assessed before and after priming. Type of priming was a significant predictor of maternal cognitions, with WRP resulting in more negative thoughts, higher thought recurrence and more self-focus relative to NP across the entire sample. Interaction effects between group and priming were significant for two parenting variables: Compared with controls, WRP had a more negative impact on maternal responsiveness to infant vocalization for GAD, and to a lesser extent for MDD; WRP led to decreased maternal vocalization for GAD. Also, mothers with GAD used stronger control after the NP than WRP, as well as compared with other groups, and overall post-priming, their children exhibited lower emotional tone and more withdrawal. Across the entire sample, WRP was associated with increased child vocalization relative to NP. This study demonstrated that disturbances in maternal cognitions, in the context of postnatal anxiety and to a lesser degree depression, play a significant role in mother–child interaction.

BackgroundPostnatally depressed mothers have difficulties responding appropriately to their infants. The quality of the mother–child relationship depends on a mother's ability to respond to her infant's cues, which are largely non-verbal. Therefore, it is likely that difficulties in a mother's appraisal of her infants' facial expressions will affect the quality of mother–infant interaction. This study aimed to investigate the effects of postnatal depression and anxiety on the processing of infants' facial expressions.MethodA total of 89 mothers, 34 with Generalised Anxiety Disorder, 21 with Major Depressive Disorder, and 34 controls, completed a ‘morphed infants’ faces task when their children were between 10 and 18 months.ResultsOverall, mothers were more likely to identify happy faces accurately and at lower intensity than sad faces. Depressed compared to control participants, however, were less likely to accurately identify happy infant faces. Interestingly, mothers with GAD tended to identify happy faces at a lower intensity than controls. There were no differences between the groups in relation to sad faces.LimitationsOur sample was relatively small and further research is needed to investigate the links between mothers' perceptions of infant expressions and both maternal responsiveness and later measures of child development.ConclusionOur findings have potential clinical implications as the difficulties in the processing of positive facial expressions in depression may lead to less maternal responsiveness to positive affect in the offspring and may diminish the quality of the mother–child interactions. Results for participants with GAD are consistent with the literature demonstrating that persons with GAD are intolerant of uncertainty and seek reassurance due to their worries.

Postnatal maternal depression is associated with difficulties in maternal responsiveness. As most signals arising from the infant come from facial expressions one possible explanation for these difficulties is that mothers with postnatal depression are differentially affected by particular infant facial expressions. Thus, this study investigates the effects of postnatal depression on mothers’ perceptions of infant facial expressions. Participants (15 controls, 15 depressed and 15 anxious mothers) were asked to rate a number of infant facial expressions, ranging from very positive to very negative. Each face was shown twice, for a short and for a longer period of time in random order. Results revealed that mothers used more extreme ratings when shown the infant faces (i.e. more negative or more positive) for a longer period of time. Mothers suffering from postnatal depression were more likely to rate negative infant faces shown for a longer period more negatively than controls. The differences were specific to depression rather than an effect of general postnatal psychopathology—as no differences were observed between anxious mothers and controls. There were no other significant differences in maternal ratings of infant faces showed for short periods or for positive or neutral valence faces of either length. The findings that mothers with postnatal depression rate negative infant faces more negatively indicate that appraisal bias might underlie some of the difficulties that these mothers have in responding to their own infants signals.