Maternal neglect: oxytocin, dopamine and the neurobiology of attachment.

Maternal neglect, including physical and emotional neglect, is a pervasive public health challenge with serious long-term effects on child health and development. I provide an overview of the neurobiological basis of maternal caregiving, aiming to better understand how to prevent and respond to maternal neglect. Drawing from both animal and human studies, key biological systems are identified that contribute to maternal caregiving behaviour, focusing on the oxytocinergic and dopaminergic systems. Mesocorticolimbic and nigrostriatal dopamine pathways contribute to the processing of infant-related sensory cues leading to a behavioural response. Oxytocin may activate the dopaminergic reward pathways in response to social cues. Human neuroimaging studies are summarised that demonstrate parallels between animal and human maternal caregiving responses in the brain. By comparing different patterns of human adult attachment, we gain a clearer understanding of how differences in maternal brain and endocrine responses may contribute to maternal neglect. For example, in insecure/dismissing attachment, which may be associated with emotional neglect, we see reduced activation of the mesocorticolimbic dopamine reward system in response to infant face cues, as well as decreased peripheral oxytocin response to mother-infant contact. We are currently testing whether the administration of intranasal oxytocin, as part of a randomised placebo controlled trial, may reverse some of these neurological differences, and potentially augment psychosocial and behavioural interventions for maternal neglect.

Childhood neglect and cognitive development in extremely low birth weight infants: a prospective study.

OBJECTIVE: To examine the relationship between child maltreatment and cognitive development in extremely low birth weight infants, adjusting for perinatal and parental risk factors. METHODS: A total of 352 infants with birth weight of <1000 g were followed prospectively for 4 years. The data were analyzed with regard to perinatal and parental risk factors and referrals for suspected child maltreatment to government agencies. Perinatal risk factors included birth weight, gestation, gender, periventricular hemorrhage, ventricular dilation, home oxygen requirement, and necrotizing enterocolitis. Parental risk factors included maternal age, race, marital status, education, and hospital insurance status. Cognitive z scores were calculated at 1, 2, and 4 years, and head circumference z scores were calculated at birth, 2 years, and 4 years. RESULTS: Fifteen percent of infants were referred to child protective services for suspected child maltreatment. The adjusted general cognitive index at 4 years was significantly reduced in infants who were referred for neglect (-17.6; 95% confidence interval: -3.3, -31.9). Infants whose neglect was substantiated had a progressive decline in their cognitive function over time (cognitive z scores: -0.97, -1.37, and -2.05 standard deviations at 1, 2, and 4 years, respectively), compared with non-neglected infants (z scores: -0.04 to -0.36). They had a significantly smaller head circumference at 2 and 4 years but not at birth (adjusted z score at 4 years: -0.812; 95% confidence interval: -0.167, -1.458). Perinatal risk factors and physical disability were not related to maltreatment referral; only parental factors were independent predictors. CONCLUSIONS: Childhood neglect is associated significantly with delayed cognitive development and head growth. Addressing risk factors antenatally and in early childhood may improve outcomes.